physiology notes semester 1

7/30/2019 Physiology Notes Semester 1

http://slidepdf.com/reader/full/physiology-notes-semester-1 1/84

1. Introduction to Physiology 9/15/2012 1:11:00 PM

Physiology

Study of function in living organisms

Mechanisms controlling internal environments regardless of what

happens in external environment – mechanisms of homeostasis

Physical and chemical factors responsible for normal function anddisease (pathology)

Homeostasis

Maintenance of relatively stable conditions within the internal

environment to ensure normal function despite a variable external

environment

o Internal environment: fluid cells are bathed in (interstitial

fluid & blood plasma) – DOES NOT INCLUDE CELLS! Just the

SPACE the cells are in

o External environment: region outside the body AND the inside

of digestive, respiratory, and urogenital tracts e.g. kidneys

and bladder (these tracts connect to the outside, but only

some are continuously so e.g. lungs)

Almost all organs within the body are involved in maintaining

homeostasis, controlled by 2 systems:

o 1. Endocrine system (hormones, slow)

o 2. Nervous system (instant)

Negative feedback control system Both systems use negative (and positive: amplify effect) feedback

control system

Set point is a desired value(e.g. 37C), controlled variable (body

temperature) detected by sensor (nervous system) and reported to

the control center (hypothalamus), which notices the difference

between current and set point value, activate effector (organs and

systems to generate heat) thus changing the controlled variable

back to the set point (37C) which SHUTS OFF the effectors (thus

negative feedback



positive feedback = controlled variable keeps control center going

Levels or organization in human body

Atoms molecules macromolecules (DNA) cellular organelles

(many similar/common in all cells, though some are highly

specialized - e.g. muscle cells has more contracting protein)



tissue (groups of cells with same specialized function - e.g. muscle

tissue) organs (two or more types of tissue form a functional unit

- e.g. heart) organ systems (several organs cooperate for a

common function - e.g. cardiovascular system = heart and blood

vessels) organism All these organ system’s 1 common function: maintain homeostasis



2. Body Fluids 9/15/2012 1:11:00 PM

Introduction

Homeostasis means volume of fluid & concentration of chemical

ions of internal environment (which is bathed in fluids) need to be

strictly controlled.

Body Fluid CompartmentsTotal body water (TBW) = 42L in average 70kg

standard man – 60%

1. Intracellular fluid (inside the cells) –

67% (by volume)

Extracellular fluid (=internal

environment of the body =everything

outside the cells)

o 2. Interstitial fluid (fluid directly

outside the cells) – 26%

o 3. Plasma (liquid portion of the

blood) – 7%

92% water and 8% other substances (proteins, ions,

nutrients, gases, waste products)

colloidal solution (containing suspended substance, such

as plasma proteins, that won’t settle out)

Plasma volume is relatively constant despite water

intake (due to water loss through kidneys, lungs,digestive tract, and skin)

Chemical Composition

Big difference in concentration between the inside and outside of

the cell (intracellular and extracellular), but small between

interstitial fluid and plasma (extracellular)

o Much higher concentrations of Na+, Ca2+, Cl- outside the cell

o Most K+ and protein ions are inside the cell

o SALTY (Na+ outside) BANANA (K+)

Difference in ion concentration caused by the selectively permeable

nature of cell membrane (the barrier between intra/extra cellular

fluid)



o Only some substances can

cross easily

o Doe this through channels,

pores, special transport

systems



3. Human Cell 9/15/2012 1:11:00 PM

Basic Cell Organelles

Nucleolus: dense body within the cell nucleus containing specific

DNA that produces the RNA found in ribosomes

Centriole: bundles of microtubules that move DNA strands during

cell division Endoplasmic Reticulum: continuation of cell’s nuclear membrane,

responsible for synthesis, storage and transport of proteins and

lipid molecules

o Rough ER: covered with rows of ribosomes (protein synthesis,

packaged into vesicles and transported to Golgi apparatus)

o Smooth ER: no ribosomes (lipids/fatty acids synthesis)

Mitochondrion: Produces ATP (energy storage and transfer) –

powerhouse of the cell

o # of mitochondria depends on cell’s energy needs

o can replicate themselves even without cellular division

Golgi Apparatus: package proteins from rough ER into membrane-

bound vesicles

o Produces both secretory vesicles (transport proteins to cell

membrane and releast into extra-cell environment) and

storage vesicles (e.g. lysosome; store contents to use within

cell)

o Lysosome: act as digestive system of cell – have enzymesthat destroy damaged organelles, bacteria, and molecules to

be broken down

The Cell Membrane

Separates intracellular environment from extracellular environment

Selectively permeable – important for intake of nutrients and

emission of waste

Made up of mainly phospholipid molecules + proteins (channels and

pores), carbohydrates (cell recognition), cholesterol (stability)

o Phospholipid molecule: phosphate polar head with lipid non-

polar tail

o Phospholipid bilayer: two layers, tail to tail to form non-polar

centre (barrier to water/water-soluable substances, e.g.

glucose, urea, ions), heads facing outside and insides of cell



Cholesterol molecule: inserted into the non-polar centre, helps to

make membrane impermeable to some water soluble molecules and

keep membrane flexibility despite temperature change

Associated proteins:

o Enzymes: found inside/outside membrane: catalyze reactionso structural proteins: usually inside surface, strengthen

membrane, anchor organelles to the inside surface

Membrane spanning protein: span entire width of the membrane,

act as gates/channels controlling movement of substances

Carbohydrate molecule: can be on membrane proteins/lipids –

forms protective layer of glycocalyx -> role in immune response

and cell-cell recognition

Membrane Proteins

Receptors: attachment of chemical hormones/neurotransmitters

Enzymes: help chemical reactions/breakdown of molecules

Ion channels/pores: allow water-soluble substances to travel

Membrane-transport carriers: transport larger molecules and

molecules against conc. grad. across the membrane

Cell-identity markers: antigens (foreign particles that stimulate the

immune system)/glycoproteins

Membrane-transport mechanisms

Endocytosis(coming into cell)/exocytosis (leaving the cell): of small molecules through transport of a vesicle (which just fuses

with membrane; content’s don’t actually cross it through an

opening)

Diffusion: movement of molecules from high to low concentration

(moving down the chemical concentration gradient), stops when

gradient is 0 and thus equilibrium (still travel, no macro change)

o Ions have both chemical gradient and electrical gradient

(opposite charges attract). The two gradients may be in

different directions, and when they balance and ions stop

moving, that is an electrochemical equilibrium

o Lipid-soluble substances can diffuse right through the cell

membrane, only controlled by concentration (O2, CO2, fatty

acids, some steroid hormones)



o Water-soluble substances (e.g. ions) can’t diffuse directly,

need specific protein channels/pores

o Diffusion factors (things that limit rate of movement through

protein channels)

Size of channels, charge on molecule and channel,electrochemical gradient, number of channels

o Facilitated diffusion: larger substances can’t pass through

protein channels, they attach to specific protein carriers which

causes the protein to change shape and let them through

Requires no energy, powered by concentration gradient

Rate of transport limited by # protein carriers

Once all carriers working, saturated, no faster rate

Protein carriers = specific, and may be inhibited

Active Transport

o Moves against concentration gradient (e.g. Na-K pump)

o Requires protein carriers, can be saturated, and shows

chemical specificity and competitive inhibition just like

facilitated diffusion, BUT USES ENERGY! (ATP)

Osmosis

Water moving down its concentration gradient across a membrane

(diffusion of water)

Happens when solute molecules can’t diffuse themselves; watermove to area of lower concentration (higher solute concentration)

Affected by

o Permeability of membrane to solutes

o Concentration of solutes (inside/outside)

o Pressure gradient across the cell membrane

Units of Osmosis: osmole (Osm)

Osmotically active particle = one that causes osmosis (e.g. Na+, Cl-

, K+, glucose)

1 osmole = 1 mole of osmotically active ion/substance

osmolality/osmolarity = sum of osmole / kg or L (sum of molarity of

ALL osmotically active ions/substances)

e.g. 1.5 M CaCl2 = 1.5 M Ca++, 3 M Cl-, total 4.5 Osm

Glucose don’t dissociate, only dissolve, so 1M glucose = 1 osm/kg

Typical human cell /body fuids = 300mOsm/kg



Tonicity: ability of solution to cause osmosis across layer

o Isotonic solution: same concentration as cell

o Hypotonic solution: lower conc. than in cell (swell)

o Hypertonic solution: higher conc. than in cell (shrink)

Concentration Gradients & Membrane Permeabilities Not very permeable to Na+, Cl- and Ca++ ions, few channels for

them on the memraben

More permeable to K+, some will leak out down its conc. grad.

There are more specific ion channels we have yet to learn

Membrane Potentials

Charge difference between the inside of the cell (-) and the outside (+)

Resting Membrane Potential

Immediately inside

the cell membrane = anions (-)

and immediately outside the

membrane = cations (+)

This potential

difference present even every

resting cell = ~ -70mV

(comparing inside to outside)

Equilibrium Potentials

o Electrochemical equilibrium: when the force of chemical conc.

grad. (drives ion from high to low conc) and electrical grad.

(drives ion toward area of opposite charge) equalize in

magnitude but opposite in direction, and no net mov. of ion.

o Equilibrium potential of an ion = electrical potential the

inside of cell (-70mV) need to be to stop movement of ion

down its concentration gradient.

E(K+)=-90mV (wants to get out, so make inside very

electrically attractive)

E(Na+)=+60mV (want to get in, so make inside

positive to keep it out)



E(Cl-)=-70mV

o Since actual resting potential is -70mV, some K+ will get out

and some Na+ will leak in, but we have pumps to balance

that

Sodium/Potassium Pumpo Integral membrane protein that pumps 3 Na+ out and 2 K+

in, making the inside more negative to reach the resting

potential of 70mV electrogenic pump

o Requires ATP since pumps both against concentration

gradients active transport

o Without it, most cells would just burst; net pumping out

means reducing particles in side so less water come in

Significance of Resting Membrane Potential

o Excitable cells can use the membrane potential to do work

Then spontaneously regenerate electrical potentials at

their membranes

Two types: nerves & muscles



4. Nerve Cells 9/15/2012 1:11:00 PM

Review: all cells have membrane potentials, inside-, outside+; maintained

by electrochemical gradients of intracellular and extracellular ions (K+

inside, Na, Cl-, Ca++ outside)

Action Potential

Nerve cells and muscle cells are considered “excitable”: use restingmembrane potential to generate an electrochemical impulse called action

potential

How nerve cells communicate with one another

Important for muscle contractions

Nerve Cell Structure

Dendrites: thin branching processes of cell body receive incoming

signals, increase overall SA to communicate. # varies depending on

where the neuron is located

Cell body: control centre of the cell, containing nucleus/organelles

Axon: carries the action potential, may or may not be myelinated

Myelin Sheath: insulator for axon, phospholipid layer, forcing ion

exchange to take place only at nodes of Ranvier

Collaterals: branchings of axon near it’s terminal end, serve to

increase number of possible target cell for neuron to interact



Action Potential



Voltage-Gated Sodium Channel: activation gate normally closed whileinactivation is opened (both gates on intracellular side). Depolarization:

activation gate opens quickly, Na+ pour into the cell until inactivation gate

closes and flow stops absolute refractory period, won’t open to fire

another action potential regardless of stimulation, then go back to normal

configuration which is inactivation gate open and activation gate closed.

Voltage-Gated Potassium Channel: only one gate, opens as Na+ gate

enters inactivated period after depolarization, K+ flow out of the cell

repolarization until gate closes and returns to resting configuration

Depolarization begins on axon hillock, has highest concentration of voltage

gated channels. When membrane of nerve cell depolarizes, Na gate open

and Na rushes in down its concentration gradient, inside becomes more

positive/depolarized rapidly to +35mV, sodium quickly becomes inactivated

(miliseconds), meanwhile potassium open, and K+ rushes out, causing



repolarization back to normal, except K gate closes but more slowly, K+

continues to rush out causing slight hyperpolarization (-90mV relative

refractory period (possible to fire another action potential if very strong

stimulus to reach threshold). Resting potential will restore through passive

movement of ions through leak channels to -70mV.

Threshold for Starting an Action Potential

Action potential only occur if almost all of the Na+ voltage-gated channels

open to form a large enough +charge = -55mV (threshold for generating an

action potential). If below, the K+ and Cl- leak channels (always open) will

make K+ go out and Cl- come in to repolarize back to normal (no AP then)

called natural repolarizing forces. If above, AP will always occur. All-or-

nothing



Round peak of action potential = N-gate beginning to close while K-gate

beginning to open (as K+ leaves and voltage go down, some Na+ still

coming in to slow down this decline initially)

Important FactsNo appreciable change in conc. grad. of ions after one action potential (very

small fraction participate in the first place). However, since only Na+ goes in

and K+ goes out, can occur thousands of times before insufficient con.gra.

between intra/extra cell. Also, the pumps aren’t required for repolarization?

Action Potential Propagation

Propagation/conduction: action potential will travel down the axon of the

nerve from hillock to the axon terminal where it will communicate with

another cell

Unmyelinated axon: initial action potential makes inside positive

+35mV (Na+ entered); positive charge moves toward adjacent, -

charged membrane and creates a local current (+ -); adjacent

now depolarizes, triggering Na+ channels to open, depolarizing the

region to threshold and new action potential fired! So on.

o The travelling is unidirectional due to inactivate voltage-gated

channels which will be in the state of absolute refractory

o Each depolarization acts as the stimulant for the next oneadjacent to it down the axon; the first is triggered by

depolarizing stimulus

Myelinated axon: insulated with fatty material myelin produced by

Schwann cells so few ions can leak through membrane. Voltage-

gated Na+ and K+ channels can only exist at gaps between the

myelin nodes of Ranvier, so each action potential moves towards

the adjacent node of Ranvier (negative) directly.

o Jumpts from one node to next saltatory conduction

o Much faster than unmyelinated fibers

Action potentials will almost always have fixed height/amplitude, since it’s

all-or-nothing (either have above threshold to reach 35 for a full potential

and pass it on or none at all) and potentials can’t overlap (abs. refractory)

Multiple Sclerosis (MS)



Myelination speeds up conduction of action potentials, but for people with

MS, immune system attacks and damages myelin surrounding axon of

nerves, can interrupt flow of action potential such that no transmission

occurs. If damaged nerve connected to a muscle, paralysis.

Synaptic Transmission

Connection between the axon terminal and another cells

(nerve/muscle/organ) chemical synapse

Neuromuscular junction (between neuron and muscle cell)

Motor nerve fiber: neuron contacting a muscle cell

Presynaptic axon terminal: axon terminal contacting muscle cell

o Contains Ca++ voltage-gated channels, also open when cell

membrane depolarizes

o Also contains synaptic vesicles containing neurotransmitter

acetylcholine (ACh), activated by inflowing Ca++

Basement membrane of axon terminal (the muscle cell-contacting

membrane) contains enzyme acetylcholinesterase (AChE)

Sarcolemma: muscle cell membrane directly under the axon

terminal

End plate: the region interfacing motor fiber/muscle cell belowsynaptic cleft (gap between the two): contains receptors for

acetylcholine – associated with ligand-gated ion channels



1. action potential arrives at presynaptic nerve fibre terminal causingvoltage-gated Ca2+ channels to open and Ca++ flow into nerve cell

2. Ca++ triggers fusing of synaptic vesicles to membrane and release Ach

into synaptic cleft (exocytosis)

3. Ach diffuses across synaptic cleft, attach to ACh receptors on muscle cell

postsynaptic membrane

4. ligand-gated (ACh is the ligand here) ion channels on muscle cell open

(Na and K gates) and Na+ flow in while some K+ leaves, local depolarization

end plate potential (EPP) not action potential, happens before it.

5. depolarization of EPP spreads to adjacent cell membrane, threshold

reached and large amounts of Na+ flows into muscle cell, triggers action

potential. Muscle cell contracts.

6. Ach broken down to acetic acid and choline by enzyme AChE, only choline

reabsorbed by presynaptic terminal to be recycled and combine with acetic

acid



note: if you have an action potential on motor nerve, always have

enough to generate an action potential on the muscle (threshold

overcame)



5. Muscles 9/15/2012 1:11:00 PM

Introduction (don’t need to know)

Muscles: utilize chemical energy from metabolism of food to perform useful

work

Skeletal muscle: voluntary motion

Smooth muscle: walls of blood vessel, airways, various ducts,urinary bladder, uterus, and digestive tract

Cardiac muscle: found in the heart

Over 600 different muscles with three principle functions

Movement, heat production, and body support/poster

Structure of Skeletal Muscle

Muscles made up of bundles of fasciculi (singular: fascicle)

surrounded by connective tissue perimysium, each made up of

groups of muscle cells (= muscle filbres), each cell contains many

bundles of myofibril containing 2 types of myofilmanets: thin

myofilaments (made up of protein: actin and troponin &

tropomyosin) and thick myofilaments (protein myosin)

Muscle contraction: interaction of thin and thick myofilaments



Structure of a Muscle Cell

>1 nucleus

cell membrane = sarcolemma , transmit action potential

o has small tube-like projections extending into the cell called

transverse (T) tubules: conduct action potential deep into the

cell where contractile proteins are located



Myofibrils are surrounded by sarcoplasmic reticulum (SR): network

of tubes containing Ca2+ ions (essential for contraction)

o Terminal cisternae: membranous enlargement of the SR

surrounding the T-tubles and where the Ca2+ are stored

Thin Myofilament

Mainly globular protein actin strung together like beads on 2 long

protein strands tropomyosin (twisted necklace), each actin molecule

contains a special binding site for the other contractile protein

myosin (on thick myofilament)

Troponin: regulatory proteins

o Troponin A: binds to actin

o Troponin T: binds to tropomyosin

o Troponin C: binds with Ca2+



At rest, tropomyosin is held by troponin complex to cover up actins’

binding sites for myosin

Thick Myofilament

Made up of protein myosin: long bendable tail and two heads (both

can bind to actin, and also can bind and split ATP)



Actin/Myosin Relationship

Z disk = where thin myofilaments are anchored and extended from

o Region from one Z disk to another is called a sarcomere: the

smallest functional contractile unit of the muscle cell

M line (vertical to length of muscle cell) = where groups of thick

myofilaments extend from

Under microscope: A band = thick filaments, I band = thin



Muscle Contraction: Sliding Filament Theory

Muscle contraction: interaction between actin/myosin

Head of myosin molecule attaches to binding site on actin forming a

crossbridge, myosin changes shape, causing its head to swing and

produce the power stroke: much like dragon boat! Slides actin past

myosin, but neither thin/thick filaments shorten during contraction,

only the sarcomere shortens; this is why entire muscle shortens

when contracted

Excitation-Contraction Coupling (what turns action potential into a

muscle contraction)



Process by which action potential coming from neuromuscular junction

spread out over sarcolemma, down to T-tubules (which are like a

continuation of the sarcolemma), into core of muscle cell to produce a

contraction. The AP travels very close to sarcoplasmic reticulum, opening

Ca2+ channels and release Ca2+ from terminal cisternae of the SR. TheCa2+ ions will bind to troponin C on thin myofilmanets and cause

tropomyosin to uncover myosin binding site of actin. Power stroke occur!

Actin-Myosin and ATP Cycle (need both AP and ATP for contraction!)

1. ATP ADP + Pi occur in ATP binding site of myosin, releasing energy to it

2. Ca2+ released from sarcoplasmic reticulum by an action potential binds to

Troponin C, tropomyosin roll off myosin-binding sites on actin

3. Powerstroke occurs, but myosin remain binded until ADP and Pi released

from myosin head and a new ATP comes in; then the cycle repeats

Relaxation of Muscle

Action potential stops, Ca2+ no longer diffuse out of sarcoplasmic reticulum,

special calcium pumps pump Ca2+ back into SR up its concentration

gradient with ATP (but only so fast since pumps can be saturated, that’s why

when we tire our muscles they don’t just relax quickly), tropomyosin will

cover myosin binding sites again. But remember: as long as there are still

Ca2+ around, the muscle will remain contracted.

http://www.youtube.com/watch?v=0kFmbrRJq4w

Altering Force of Contraction (how we can lift different weights)

2 ways to increase tension (force of contraction): increasing voltage by

recruiting more motor units and putting them to work, or increasing

frequency of action potential and summing twitch contractions

1) Recruit motor units

Motor unit: motor neuron and all the muscle cells it causes to contract (each

cell innervated by only one motor neuron); number of cells a neuron controls

varies, from a few to 200+

2) Summation Twitch Contractions

Muscle twitch: from one action potential in motor neuron, simplest and

smallest muscle contraction






Twitch Duration=10-100ms, where as duration AP is 2ms; this

means you can have multiple AP during one twich, between 5-50!

And all of them can add up.

Latent period: time delay from when AP occur on motor and to

muscle contracts; caused by events at neuromuscular junction,generation of AP on muscle cell, thin and thick myofilaments

interactions

Increasing the frequency of action potentials = stimulus (until the max of 1

every 2ms) can increase force of contraction: summation of twitch

contraction, caused by the fact a twitch has longer duration than AP. Can’t

be summed up in neuron due to absolute refractory period caused by

inactivation of Na+ v-gated channels.

Maximal tetanic contraction: reached at high frequencies shown by

plateau in muscle tension; no relaxation at all



6. Nervous System 9/15/2012 1:11:00 PM

Introduction – Nervous System

1. central nervous system (CNS)

brain and spinal cord

2. peripheral nervous (PNS)

others nerves - outside the CNS (go to muscles/organs like heart)o somatomotor nervous systems (going to skeletal muscles) –

somatic motor system

o autonomic nervous systems (other organs like heart )

Basic Structure of the Brain

Two cerebral hemispheres (left and right)

o left hemisphere sends signals to right side, and vice versa

o each hemisphere = divided up into 4 lobes with specific

functions: frontal lobe, parietal love, temporal lobe, occipital

lobe

brain stem: controls some of the most basic functions (heart

rate/respiration)

o contains midbrain, pons, and medulla oblongata

o medulla = continuous with the spinal cord

Cerebellum: responsible for coordinated movement

Diencephalon: thalamus & hypothalamus

Bumps = gyri, dips = sulci increase surface area

Neurons and Glial Cells (makes the brain)



Glial = 90% of the brain provides environment for the neurons

Maintain delicate internal environment of the CNS

Gluing things together, regulate the nutrients & environment

Regulate passage of substances between blood / brain’s interstitial

space Astrocytes, microglia, and oligodendrocytes (produce myelin)

Neurons = information transmitting/processing cells

Bipolar neurons: 2 processes extending from cell body (e.g. retina)

Unipolar: one process extending from the cell’s body (peripheral

nerves outside the CNS) generally sensory/transmit signals

to/from spinal cord (body lies off to one side of axon, but middle)

Multipolar: many branching dendrites (most common in CNS)

Languages of Nervous System / Neural Coding

Information travels down axons in the form of an action potential

Neural coding: the stronger the stimuli (heavier it is) the more

action potential per second (higher frequency)

Synaptic Transmission: the chemical synapse



The way nerve cells communicate with one another (similar to

neuromuscular junction)

neurons meet with each other via axon terminal of one neuron

(presynaptic neuron – “before synapse”) releasing neurotransmitter

chemical to and meeting with dendrites of another neuron(postsynaptic neuron – “after synapse”)

1. presynaptic neurons makes neurotransmitters – stored in synaptic

vesicles and

2. action potential travel to presynaptic neuron depolarizes membrane,

opens voltage-gated Ca++ channels Ca++ flow into axon terminal along

the concentration gradient release of the neurotransmitter from the

synaptic vesicles into the synaptic clef (exocytosis)

release of neurotransmitter is triggered by Ca++ ion influx

3. neurotransmitter cross the synaptic cleft, bind to chemical receptors on

postsynaptic cell membrane that are associated with opening of chemically-

gated ion channels positive ions flux in (Na+)



Neurotransmitters

Chemicals released by neurons at their axon terminals stored in

synaptic vesicles released in response to action potential and

causes response in postsynaptic neuron

o Excitatory – depolarization – may fire an action potential(glutamate)

o Inhibitory – hyperpolarization – decreases chance of firing

action potential (gamma-amino-butryic acid GABA)

Unlike in neuromuscular junction (NMJ), neurotransmitter doesn’t

have to be acetylcholine

o Norepinephrine (amine), GABA (aa), glycine (aa),

neuropeptides

Major different from NMJ: rather than a single AP in motor neuron

ALWAYS producing a single AP in muscle cell, at chemical synapse,

single action potential on presynaptic neuron will NOT produce an

action potential on a postsynaptic neuron.

o Note: 1 neuron only releases one specific neurotransmitter

Excitatory postsynaptic potential - EPSP

Excitatory Neurotransmitters are released from presynaptic neuron

and bind to their receptors causing chemically gated channels to

open + ions (Na+ mostly) flux into dendrites local

depolarization of membrane = EPSP (excitatory postsynapticpotential) – very local event like End-Plate Potential; but EPSP

diminishes (with time & distance)

still no AP (action potential) yet though – need voltage-gated

channels to open = essential for AP production

o most V-gated channels = found at axon hillock, so EPSP must

be strong enough to depolarize all the way to there

o there’s no v-gated channels on dendrites/cell body

Increasing strength of an EPSP (both = additive effect)

o Spatial summation of EPSPs: many EPSPs generated at many

different synapses on the same postsynaptic neuron at the

same time

o Temporal summation of EPSPs: many EPSPs generated at the

same synapse by a series of high-frequency Aps on the

presynaptic neuron



o Both can help the EPSP travel to axon hillock and open a

sufficient number of v-gated channels to reach threshold

(from -70mV to -55mV) and fire the action potential

Inhibitory Postsynaptic Potentials – IPSP

Stimulus causes a hyperpolarization by opening different chemically

gated channels that let Cl- in or K+ out (either way making the

inside/membrane potential more negative) hence hyperpolarization

o Makes membrane potential even further away from threshold

shut off the nerve cell

Summation (spatial and temporal) can also occur in IPSP (since the

only difference is which chemically gated channels they open on

postsynaptic dendrite) produce larger hyperpolarization



Important*: one neuron will ONLY RELASE ONE SPECIFIC

NEUROTRANSMITTER. It’s not like they can choose. But brain can choose

which neuron to activate to achieve desired effect

Properties of EPSP and IPSP (they =/= action potential!)

Occur in dendrite region of neuron (localized!) – must spread toaxon hillock, by the time of which if depolarization still large enough

to make mem.potent.> (-55mV), FIRE! (ap = only on axon)

Can have varying sizes, big or small (change by 1mV or 10mV,

sure!) (ap = “all or nothing”)

Spread but decay over distance & time – fades away like ripples

Can be summed: temporal (throwing rocks one after another to the

same spot) or spatial (throw whole bunch of rocks at the same

time) (ap cannot be added due to refractor period)

Can be integrated/combined (>1 presynaptic neuron on one

postsynaptic neuron, some firing EPSP some firing IPSP = signals

battle / stronger wins / cancel out in postsynaptic neuron)

o THIS BATTLE = SYNAPTIC INTEGRATION



The Somatic Motor System

How the brain controls muscles to perform voluntary movements (brain part

responsible for activating muscles, spinal tract which sends the info down,

and muscles send sensory info back to brain)

Structure & Organization of Motor System

Premotor cortex,

Supplementary Cortex,

primary motor cortex =

in the frontal lobe



1. The Premotor Cortex

e.g. picking up a coffee cup

decision comes from

prefrontal cortex passes

signal to premotor cortex

(frontal lobe): determines

the way an action will be

carried out / develops

strategy for movements

necessary for action (how to

move which muscle group in

what order)

after sequence of muscle contractions developed, pass this to supplementary

2. The Supplementary Motor Cortex

programs the motor sequences – the more complex/repetitious the

movement, the more important to have the supplementary motor

cortex’s role program written, sent to primary

3. Primary motor cortex

activate the neurons that will eventually activate the appropriate

muscles

arranged in a specific manner as if entire body was projected onto

the surface of the brain like a map topographical representation

= motor homunculus (specific area of motor cortex activates a

particular muscle)

4. Cortico-spinal Tract

major motor pathway from primary motor cortex to motor neurons

(which communicates with muscle cells)

tract begins in primary motor cortex, down to brain stem, and enter

the spinal cord and down until they synapse with motor neurons

(directly contacting the muscle at corresponding places in body)



In medulla (inside brain stem): 80% nerve fibers cross over to

contralateral side (the other side of the body), the other 20%

originally ipsilateral nerves will cross over to contralateral side as

they reach their destination in spinal cord

5. Muscle Receptors send signals back to the brainproprioception: awareness of the positions of the limbs and extent of

muscle contract at any given time muscle sense (e.g. touch 2 index

fingers close-eyed) allows us to make movements without looking

constantly

only possible due to muscle

receptors:

1. muscle spindles: detect

length and stretch of muscle &

rate of change in muscle length

2. Golgi tendon organs: detect

muscle tension

1. Muscle spindles: series of

intrafusual fibers (inside the

extrafusal fibers: real contractile

muscle cells), (central) sensory

region, 2 sets of gamma motor

neurons, and sensory neuron

that originates in sensory region

When muscle stretches, so does

sensory region of spindle,

depolarizes & triggers action

potential in the sensory nerve,



sending signals to brain (more stretch = more depolarization = more AP);

brain can decipher how stretched the muscle is AND relative position of limb

in space attached to the muscle (proprioception)

alpha-gamma coactivation during contraction: signals from CNS travelthrough alpha motor neurons in extrafusal fibers to cause muscle

contraction – during which gamma motor neurons also send signals to

contract intrafusal fibers so it can continue to send info to brain (or else it

goes into slack and stops working)

The reflect arc: a most basic example of integrated neural activity – NO

BRAIN INVOLVED.

Receptor (skin) receptor potential action potential in afferent

neuron spinal cord, causes AP there and on interneurons AP in

efferent neuron activate effector (like muscle)

Does not require output by brain, goes to brain but only because

that’s already the shortest path connecting receptor & muscle

Stretch Reflex

An example of reflex arc found in all muscles (here = quadriceps muscle)

Tapping tendon small stretch in muscle stretch in muscle

spindles which triggers AP in afferent neuron entering spinal cord

efferent = quadriceps contract while hamstring relax lower legs

kicks out



Cerebellum – “little brain”

Contains more neurons than the rest of the brain combined!

Contribute to generation of accurate limb movements, correctingongoing movements, modifying strength of some reflexes

o Receive and compares info from 2 sources: signal from

primary motor cortex travelling out to muscles &

proprioception (position of limbs in space) back to brain

should match, and if not, cerebellum modify signals from

primary motor cortex

Involved with learning of new muscle movements

Vestibular ocular reflex (staring at one spot while moving your head

LOL)

Limbic System & Hypothalamus (emotional centre & hemeostasis ctrl)

Both of these regions together coordinate variety of autonomic,

hormonal, and motor effects associated with hemeostasis and

emotional behaviours (eating, drinking, sex, attack memory)

Limbic System



Composed of hypothalamus, amygdala, hippocampus, and cingulate

cortex (and septum) forms ring around brain stem

Link higher thought processes of brain with more primitive

emotional response of fear/rage/sexual pleasure

Linked to feeding, drinking, pain, motivation, learning Respond correctly to changes in our environment

Hypothalamus

Based of brain anterior to brain stem – small portion, yet importantfunctions

A major regulator! Regulates temperature control, body water, food

intake, cardiovascular, circadian clock, and coordinates emotional

behaviours, controlling hormones released from pituitary gland

(mostly negative feedback control)



The Pituitary Gland

Also small and important (only s small pea-sized thing below

hypothalamus

Control and release hormones – closely regulated by hypothalamus

The Autonomic Nervous System (ANS)

Unlike somatomotor system, not under voluntary control

Controls heart rate, pupils in eyes, smooth muscle in walls of

arteries/veins, glands and other organs

2 divisions: sympathetic and parasympathetic nervous system;

each system sends neurons to each of the organs (adrenal = only

SYN) the two always work in opposite in an organ – of one excite

the other inhibit

Sympathetic (SYN)

Activate body functions of fight or flight situations

Increase heart rate/BP, dilate airways and blood vessels to muscles,

shut down digestive system

Parasympathetic (PSYN)

Storage & conservation of energy – rest and relaxation



Neurotransmitters of ANS

Both use acetylcholine (Ach) between preganglionic/postganglionic neuron,but SYN uses norepinephrine (NE) onto target organ as well as Ach while

PSYN only uses Ach.



7. Sensory Systems 9/15/2012 1:11:00 PM

Intro

To maintain homeostasis (stable internal environment despite external

conditions) body needs to detect changes in external environment to react

appropriately sensory systems!

Somatosensory system (touch) Visual system (vision)

Auditory & vestibular system (hearing)

Olfactory system (smell

Gustatory system (taste)

Transduction of environmental information

Translating the information about external environment into

language brain understands: action potentials

Environmental stimuli (light/heat/touch/sound) detected by sensory

receptors, convert into action potentials

Environmental Stimuli: converts stimuli to AP

Mechanical stimulus: touching/vibrating the skin – stretch sensory

receptors in skin and open ion channels depolarization of sensory

neuron to produce AP

Chemical stimulus: sour taste / odor in nose – binds with receptors

to cause depolarization and AP

Light energy: absorbed by photoreceptors of eye (retina’s rod and

cone cells) AP Gravity and motion: detected by hair cells in vestibular system AP

Adequate Stimulus: the stimulus a receptor’s particularly good at detecting –

specialized to be the most sensitive to it

E.g. adequate stimulus for rod and cone cells of retina is light

However, receptors can sense more than 1 type of stimuli; rod and

cone can also sense pressure

Receptor Potentials only occur in receptors, after they are stimuluated

Similar to the way excitatory neurotransmitter produces EPSP at chemical

synapse which then generates AP at axon hillock if strong enough

Sensory receptor stimulated by environmental stimulus change

in ion permeability causes local depolarization called receptor

potential in the receptor cell



Receptor has no voltage-gated ion channels, no AP, so receptor

potential need to spread to a sensory neuron which has v-gated

channels; usually first node of Ranvier on the axon AP generated

and propagated along axon into spinal cord

Many similarities with EPSP & IPSP, shared characteristics include Generally depolarizing but can be hyperpolarizing as well

Caused by an increase in permeability to Na+ ions (or K+ for

hyperpolarizing stimulus)

Local and don’t propagate down the neuron like AP; spread and

decrease in strength with time/distance from stimulus

Potential strength is proportional to strength of stimulus thus

likelihood of firing an AP

Receptor Potential & Neural Coding

Heavier weight trigger receptor to produce larger receptor potential

trigger more AP on sensory neuron’s axon high-frequency AP

reaches brain (process of conveying weight to brain using AP

frequency = neural coding)

Somatosensory System

Detects and processes sensations of touch, vibration, temperature and pain

(mostly from skin) – each sensation requires a few different sensory

receptors, but skin receptors collective called cutaneous receptors:

Hair follicle: receptors sensitive to fine touch and vibration Free nerve ending: respond to pain and temperature (hot/cold)

Ruffini’s corpuscles: detect touch

Meissner’s corpuscles: detect low-frequency vibrations (30-40

cycles/sec) and touch

Pacinian corpuscle: detect high frequency vibrations (250-300

cycles/sec) and touch



Receptive Field (of a receptor): area on surface of the skin where an

adequate stimulus will activate a particular receptor to fire an AP in neuron

If cells outside of the receptive field is stimulated no AP produced

Somatosensory Pathways from Periphery to Brain

How receptors deliver information/AP up to the brain (2 pathways)

1. Spinothalamic TractTransmits information of basic sensations (pain, temperature, crude touch)

Information in Sensory neuron (= lower spinal cord, 1st order

neuron) upper spinal cord (1st synapse with 2nd order neuron),

crosses to contralateral side ascends to thalamus: relay station

for all senses except smell 2nd synapse with 3rd order neuron

somatosensory cortex

2. Dorsal Column, Medial Lemniscal System

Transmits information associated with more advanced sensations (fine

detailed touch and vibration, proprioception, and muscle sense)

Same as spinothalamic tract EXCEPT don’t cross in lower spinal

cord, travels up spinal cord and cross in upper spinal cord after the

synapse with 2nd order neuron thalamus & synapse into 3rd order

neuron somatosensory cortext



*somatosensory = for sensory information, motor = for voluntary movement

info

Primary Somatosensory Cortex

the purple thing in parietal lobe behind central sulcus – where sensory

information 1st reach the brain

The primary somatosensory cortex, just like primary motor cortex, has a

topographical representation of the entire body on its surface like a map

somatosensory homunculus (vs. motor homunculus)

Not to scale, some places require processing of more sensory

information (hands, tongue, lips – the sensitive parts, also have

more receptors) and has a larger proportion in homunculus

The Visual System

Consists of the eye (photoreceptors: light AP), visual pathway

(transmits AP to brain), primary visual area (in occipital lobe of the

brain which processes the incoming signals)

The Eye



A camera: light cornea (amount of light passing through

regulated by iris) flips the light upside down focus onto retina at

back of the eye, whose photoreceptors called rods and cones

center of vision = focused onto a part of retina = fovea (highest

concentration of cone cells)

Rods cells & cone cells – the photoreceptors of the Eye



Rods

Extremely sensitive to light so functions best under low light

Only 1 type of photopigment, do not detect colour

Found mostly in the region on retina outside/around fovea

Cones Functions best under bright light, ideal for detecting detail

3 types of cone cells each with different photopigment sensitive to

their own primary colour

located in fovea (large concentrations)

both don’t have axons, so don’t generate AP, only receptor potentials that

causes release of inhibitory neurotransmitter from their synaptic ending

IN THE DARK

Other cells of the Retina

Pigment layer on retina at very back of eye of other cells to absorb

excess light (bipolar cells, ganglion cells, horizontal cells, amacrine

cells) and combines with rods/cones to produce action potential

Transduction of Light to Action Potentials – weird



Dark: cone & rod cells naturally depolarized because Na+ is flowing into

them release inhibitory neurotransmitter when no light, bipolar cells

inhibited and no AP no image

Light: strikes rod&cone cells = close their Na+ channels only, but K+ can

still leak out as usual, cell hyperpolarizes, no inhibitory neurotransmitters,means bipolar cells can depolarize spontaneously without inhibition and AP

fired in ganglion cells image!

Types of Eye Movements

We need to move our eyes in a number of ways to focus light from particular

object onto fovea

Saccades: rapid jerky movements (reading words on your

computer)

Smooth pursuit: smooth movement of eye following a moving

object (watching a plane in the sky while keeping head still)

Vestibular ocular reflex: focus on an stationary object while

shaking your head

Vergences: object moving away (eyes diverge) /approaching you (

斗鸡眼 – converging)

The Auditory System

Converts sound waves into AP and travel to the auditory system of the brain our most acute hearing occurs in range 1000 – 3000 Hz

Structure

1. External (outer) ear: the physical ear and the external auditory canal

2. Middle ear: eardrum (tympanic membrane) and

3. ear ossicles (3 bones connected like a lever system: malleus, incus,

stapes), and 6. Eustachian tube

4. Inner ear: vestibular apparatus (sense of balance) and

5. cochlea (processing sound)



Structure of the Cochlea

shell/garden snail, with the inside hollow area divided into 3

compartments/duct: upper=scala vestibule (vestibular duct),

middle = cochlear duct (insert basilar membrane here in between

middle & lower - contains organ of Corti) lower = scala tympani

Sound waves vibrate basilar membrane, bend hair cells on it



Sound: only when the wave of air pressure hits parts of the ear/microphone

does it turn into electrical information (AP) and interpreted as sound, so if a

tree falls and no one hears it, no sound created, only air waves

Sound frequency: number of sound waves per unit time

Sound intensity (loudness): amplitude of the sound waveTransfer and Amplification of Sound Vibrations

airwaves travel through air,

reach outer ear, funneled into

external auditory canal, strike

tympanic membrane, vibrates

back and forth while the ear

ossicles amplifying the pressure

waves through its levering action

Stapes causes oval window

(much smaller than tympanic

membrane) to vibrate, waves

amplified 15-20 times now due

to levering and membrane size

difference



Fluid inside cochlea (perilymph) transmits waves to hair cells

embedded in basilar membrane detect vibrations and turn them

into AP in the auditory nerve

Basilar (Basement) Membrane

Wide and thin and at top of cochlea while narrow and thick at base(near oval window); tension also varies along its length (loose at

top and tight at base)

Low frequency stimulate hair cells the top (loose), high frequency

stimulate hair cells near oval window how we can detect diff freq.

(also length/stiffness of hair cells differ)

Sound: vibration AP

When basilar membrane vibrates, hair cells bend, ion channels

open, cells depolarize, neurotransmitter releases from hair cells,

neurons of auditory nerves excited and fire AP Louder sound = stronger vibration = more bent the hair cells =

more neurotransmitter = higher frequency of AP

Signals flow to auditory cortex in temporal lobe of brain

Vestibular System

Inner ear next to cochlea maintaining balance, equilibrium,

postural reflexes by detecting linear & rotational motion

Detect linear and rotational motion + position of head relative to

rest of body + vestibular ocular reflex

Structure

Semicircular canals: detect rotational and angular accelerations of

head

o 3 of these canals, one for each plane of motion

o canals filled with fluid (endolymph)



o end of canal = ampula (a swelling) inside of which is crista

ampullaris (sensory region) contains sensory hair cells

fixed at base and top embedded in gelatinous cupula

o example: turn your head left = horizontal rotation,

endolymph inside canals will seem to move to the right, hitscupula and bends hair cells embedded in it – when bending in

a specific direction, hair cells depolarize and fire AP (bent to

opposite direction = hyperpolarize)

o



o Otolith organs: detect linear accelerations

o 2 of these, detect acceleration in vertical plane and horizontal

plane, as well as position of head when tilted

Utricle detects horizontal acceleration/deceleration (e.g.

in a car) (UH – university hospital LOL)

Saccule detects vertical acceleration/deceleration (e.g.

in an elevator) Both together detect head tilts

o Each otolith organ contain many hair cells anchored at base

and top embedded in gelatinuous membrane which has otolith

crystals in it for added weight/inertia



o

o at rest: AP produced in vestibular nerve

o accelerating vertical/horizontal plane: otolith crystals lag

behind, move in opposite direction to acceleration bends cilia of hair in opposite direction of acclereation

and cause them to increase frequency of AP in

vestibular nerve (in proportion ot acclereation)

o Note: travelling at constant velocity = feels nothing

o Decelerate: bend in the forward acceleration direction, AP

decrease further from resting state (more rapid deceleration

= lower AP frequency)

The incredible hair cell

o They are involved with processing sound by auditory system,

as well as balance/equilibrium by vestibular system

o When at rest, hair cells release small resting level of

neurotransmitter from base onto sensory nerve AP there



o When stereocilia (top) bend toward the larger kinocilium

(below it) like during an acceleration, hair cell releases more

neurotransmitter more AP

o When stereocilia bend away from kinocilium (deceleration),

releases less neurotransmitter less AP

Receptors don’t produce AP!



8. Circulatory System I: The Heart 9/15/2012 1:11:00 PM

The Heart

Size of your fist, sits in chest cavity between lungs

4 principal functions of cardiovascular system:

o transports oxygen and nutrients to all cells of body

o transports CO2 and waste products from cellso helps regulate body temperature and pH

o transports and distributes hormones and other substances

Anatomy – The Heart

2 side-by-side pumps:

right atrium and ventricle: pumps blood to lungs

left atrium and ventricle: pumps blood to rest of the body

o left ventricle’s wall is much thicker than right ventricle’s since

it needs to contract more forcefully to pump blood for body

Valves: ensure one-way flow of blood through heart

Right atrioventricular valve (R-AV valve) = tricuspid valve

Left atrioventricular valve (L-AV valve) = bicuspid/mitral valve

2 valves in each ventricle only (left and right AV valves for blood

coming in and pulmonary valve in right ventricle and aortic valve in

left ventricle for blood going out)

Circulation Through the Heart

Blood enters heart at right atrium after flowing through body

Pass through right atrioventricular valve right ventricle Right ventricle contracts, ejects blood out of heart through

pulmonary valve into the pulmonary artery to lungs

Blood in lung, CO2 out, O2 in

Blood returns to heart through pulmonary vein into left atrium

From left atrium left ventricle through the left atrioventricular

valve

Left ventricle contracts, blood ejects through aortic valve into aorta

out to the body



Myocardial Cells (myo = muscle, cardio = heart) of the Heart

1. contractile cells: similar to skeletal muscle cells, forms most of the walls

of atria & ventricles

features and contract almost same as muscle fibers

o same contractile proteins actin and myosin, arranged in

bundles of myofibrils and surrounded by sarcoplasmic

reticulum

difference



o have only one nucleus, but far more mitochondria (make up

1/3 of volume!)

o extremely efficient at extracting oxygen (around 80% of the

oxygen from passing blood, 2x of normal cells)

o cells much shorter, branched, joined together by specialstructures called intercalated discs

Intercalated discs have

o Tight junctions: bind cells together

o Gap junctions: allow for movement of ions and ion current

between myocardial cells heart can conduct AP from

cell to cell without nerves! extremely important



o 2. nodal/conducting cells: similar to nerve cells, contract only very weakly

self-excitability system: they are able to spontaneously generate AP

(thus heart impulse) without nervous input (like regular neurons)

o origin for AP: sinoatrial node (SA node) – first area to

spontaneously depolarize and make AP, called the pacemaker

of the heart (in upper posterior wall of right atrium

o AP then travel through atria to atrialventricular node (AV

node) bundle of His purkinje Fibers ventricular muscle



o transmission system: can rapidly conduct AP to atrial and

ventricular muscle too – carry impulses throughout the heart

SA Node Action Potential

All cells of heart can generate AP spontaneously, but SA node = fastestReview: these ions also

responsible for AP in heart (except

AP begin by itself)

Na+, K+, Ca++ most important



The Na+ permeability in node is higher, so Na+ will move into the

cell down its concentration gradient (same as Ca++) and cells are

slightly more positive over time initial depolarization (not AP)

K+ (trying to leave cell) permeability in SA node decrease over

time, and Na+/K+ pump pumping K+ into cells together,spontaneous AP!

Na+ and Ca++ flowing in, K+ build up inside, membrane potential

of SA: -60 mV -40mV (threshold for these cells)

o Completely spontaneous, so SA nodal cells don’t have a stable

resting membrane potential

o Slow depolarization always = pacemaker potential

Once -40mV reached, voltage-gated Ca++ channels open

o Ca++ rapidly flow in, depolarization phase (of actual AP)

o Close when voltage-gated K+ channels open (K+ go out of

cell to repolarize) return to lowest value of -60mV.

Repeat.

o (similar to neural AP, except Ca+ replace Na+ flow in and the

values are different)

Conducting System of Myocardial Cells

AP speeds up through atrial muscle AV node (conduction is the

slowest here!!! need to slow it down to ensure atria finished

contracting before ventricles start, or else WHERE TO GO?!) reach base of heart through Bundle of His (faster, takes AP to

bottom of heart apex) Purkinje fiber then spread AP throughout

ventricular muscle (fast here; ventricular muscle contracts from

apex upward so blood can be forced up and out through valves at

top of ventricles) IT’S LIKE SQUEEZING UP TOOTHPASTE!

Electrocardiogram (ECG)

Heart sits in conducting fluid, good conductors of electricity and electrical

current can be spread to surface of body

Can measure electrical potentials generated by heart by placing

electrodes on skin around heart electrocardiogram (ECG)



P wave = depolarization of atrial muscle leading to its contraction

o No wave for repolarization of atrial muscle

QRS complex = depolarization of ventricular muscle prior to its

contraction

T wave repolarization of the ventricular muscle as it relaxes

The Cardiac Cycle

All the mechanical, electrical, and valvular events taking place in heart

during a single contraction

5 steps: systole = contraction, diastole = relaxation

1. Atrial systole

AV valve open! Atria depolarizes (P) and contract; lime higher than red

because atrial pressure > ventricular pressure, but latter increases with



atrial pressure as does ventricular’s volume (increase to end diastolic volume

– 100% of max ventricular volume; EDV!)

2. Isovolumetric ventricular contraction (early ventricular systole)

Ventricles depolarizes (QRS complex) then contracts, ventricular pressure

up up up, mitral valve is closed (so blood don’t flow back to atrium) and

isovolumetric meaning no change in ventricular volume (aortic valve still

closed because pressure inside arota > ventricular pressure still)



3. Ventricular Systole (ejection period)

ventricles keep contracting this phase starts @ the breaking point when

ventricular pressure > aortic pressure = 80mmHg aortic valve opens,

blood flows into aorta ventricular volume decreases as blood pours into

aorta while pressure continues to go up to 120 mmHG until aortic valve

close when ventricular pressure < aortic pressure again (end systolic

volume, lowest pt)



4. Early Ventricular Diastole (isovolumetric relaxation period)

Ventricular pressure < aortic pressure and keeps falling as ventricle relaxes;

both valves closed and no change in volume (stays at the minimum – end

systolic volume – ESV!)



5. Late ventricular diastole (ventricular filling period; longest phase)Ventricular pressure < atrial pressure now, mitral (AV) valve open and blood

flows into ventricle, ventricular volume increases (important! 70% of

ventricle is filled during this time! Even though atrium not even contracting,

just the AV valve open and higher pressure in atrim) get ready for P wave

again when atrium contracts (the other 30% goes in). repeat.



Heart Sounds Come from closing of the heart valves (and surrounding fluid’s vibration)

1st sound: closure of AV valve (lub)

2nd sound: closure of aortic and pulmonary semilunar valves (dub)

Mechanical Performance of the Heart

1. Cardiac output (CO): amount of blood each ventricle can pump in 1

minute (around 5L at rest, if vigorous exercise: 20L – 40L both SV/HR ^)



HR = bpm

SV = vol. of blood pumped by one ventricle per heart beat

2. Control of Heart Rate Overview

Controlled by all 3 nervous systems

1. Autonomic nervous system (ANS): we already know

2. Parasympathetic nervous system (PSYN): mainly in SA and AV nodes, less

in atrial and ventricular muscles (mostly SA node though)

Decrease heart rate and force of contraction

If all 3 removed, intrinsic HR = 100bpms, but in individual, PSYN

constantly slowing heart rate to 70 bpm: called vagal tone (vagus

nerve transmits the “slow-down” signals from PSYN to SA node)



3. Sympathetic nervous system (SYN): distributed always same as PSYN but

stronger innervation to ventricular muscle

opposite effect, increase HR and force of contraction

3. Parasympathetic Nervous System when PSYN’s neurons to the heart activated: acetylcholine released

as the neurotransmitter onto SA and AV nodes causes K+

channels to open (let more K+ out)

o 1. membrane potential hyperpolarize

o 2. slope of pacemaker potential decrease (can’t depolarize as

fast, takes longer to depolarize HR goes down )

Slow down AV too (and not just SA) because you need to slow

down the conduction of AP through the heart too to ensure atria

have enough time to finish contraction before ventricules starts

Notice: lowest membrane potential = -60, threshold = -40 (no

resting potential)

4. Sympathetic Nervous System

release neurotransmitter norepinephrine (+ epinephrine/adrenaline)

onto SA and AV node (both nodes; same reason as above, speed up

both atria and ventricles) cause opening of Na+ and Ca++

channels, enter cell, reach threshold faster, rapid depolarization

heart rate go up



5. Stroke Volume

EDV = End Diastolic Volume: amount of blood in ventricle at end of diastolebefore contraction (max; 120mL at rest)

During stage 1: atria systole; after receive blood from atrium, and

ventricle pressure > atrium (AV valve closed)

ESV = End Systolic Volume: just after a systole/contraction (min; 50mL at

rest) During stage 4: early ventricular diastole period (isovolumetric)

after it gave blood to aorta and both valves closed before pressure

is less than atrium’s SV = different between the two

Note:

- if 1 one-way valve 2; valve only open when pressure 1 > pressure 2 - EDV (diastolic big volume); ESV (Systole small volume)

Factors that change stroke volume



Changing force of contraction = changing stroke volume 1. Input from autonomic nervous system (PSYN or SYN)

a. PSYN: release of acetylcholine onto cardiac muscle decrease

amount of Ca++ entering cell (slows down depolarization)

decrease force of contraction, stroke volume goes downb. SYN: release norepinephrine onto muscle cells (increase amount of

Ca++ entering the cells) increasing stroke volume

2. EDV and preload: (more blood to be pumped; higher EDV = pump harder

= less blood left; lower ESV) Frank-Starling Law of the Heart (don’t

need nervous system imput!)

a. Preload: load on heart before it contracts (amount of blood in

ventricle that stretches muscle of heart) = EDV

b. Higher load = more Ca++ channels opened to let Ca++ in, more

forceful contraction, more blood ejected

3. Changing EDV

Squeeze veins more to increase venous return (blood return to heart by

veins, which contain 70% of total blood volume)

a. do it by activating SYN (innervates smooth muscle located in walls

of veins) contract muscle around inside of vessel wall (veins have

valves to prevent backflow) squeeze more blood back to heart

EDV go up, SV go up, CO go up.

b. By exercising: contraction and relaxation of skeletal muscle alsosqueeze veins since veins run between large muscle groups same

effect, so exercising increases cardiac output!

c. By breathing more deeply (will cover in respiratory system)



9. Circulatory System II: Blood Vessels 9/15/2012 1:11:00 PM

Anatomy

Arteries and arterioles: transport blood away from heart

Large arteries branch into smaller arteries smaller arterioles

capillaries

Capillaries: gas exchange (smallest blood vessels)Veins and venules: return blood back to heart

Capillaries converge small venules larger and larger veins

2 principal loops:

pulmonary circulation: right side of heart arteries lungs

branch into pulmonary capillaries and gas exchange takes place

venules veins left side of heart

systemic circulation: left side of heart oxygenated blood

pumped out through aorta into arteries arterioles capillaries

gas exchange (O2 nutrients hormones out, CO2 and waste in)



deoxygenated blood returns through venules and larger veins to

right side of heart

Blood Volume Distribution

Total blood volume = 5L 70% in veins (thus veins called capacitance vessels)

10% arteries

15% heart and lung

5% capillaries

Blood velocity and cross-sectional area of vessels

As you go from arteries to

arterioles to capillaries,

TOTAL cross-sectional area

become larger, blood

pressure and blood velocity

both drops (flow high to low

pressure, and fast velocity

in arteries to distribute

blood throughout the body

quickly)

From capillaries to venulesto veins: cross-sectional

area decreases, but blood

velocity goes up while

pressure doesn’t.

Pressure, Flow, and Resistance

Pressure gradient: driving force of blood circulation; pressure drops

throughout the flow so blood can keep moving



Resistance: friction between blood and walls of vessels (laminar flow = flow

through a tube with non-uniform velocity - decreases @ closer to the walls)

p1-p2 = pressure

gradient (two pointsalong the tube)

Resistance increase

with

1. thicker fluid (blood

doesn’t really change in

viscosity though;

dehydration)

2. longer vessel (blood

vessel doesn’t change

length either;

overweight = stretch

them)

3. smaller inside diameter (cross-sectional area) = increased resistance!

For this course: *memorize!

larger the blood vessel, more flow (volume/time)

Control of Blood Flow in the Body

Since blood pressure usually constant, best way to regulate blood flow is by

changing radius of vessels – generally of arterioles (their ability to constrict

and dilate to a large degree)

Total flow doesn’t change though; constrict one arteriole means

increase flow in other ones to maintain constant flow

Changing Blood Flow for Needs of an Organ



Organ’s blood needs depend on its oxygen/nutrients need (e.g. after meal

blood diverted from muscle to intestines to help digestion; converse when

exercising)

Vasodilating where blood flow need to increase and or

vasoconstricting arterioles to decrease flow thereBlood Pressure and Resistance throughout the Systemic Circulation

Systolic pressure: when heart contracts listen to sound when

blood enters squeezed area (higher pressure)

Diastolic pressure: when heart relaxes listen to sound when

blood flow becomes laminar again (lower pressure)

The 120/80 we measure are of the aorta

As distance from left ventricle increases, pressure falls. By the time blood

reaches right atrium, pressure almost 0 mmHg.

Structure of the Blood Vessel



Both arteries and veins = 3 layers

Outer layer = fibrous connective tissue

Middle layer = smooth muscle and elastic tissue

Inner layer = endothelial cells

Veins has extra valves = ensure blood flows one direction back to

the heart

Capillary: just a single layer of endothelial cells permits diffusion

Also clefs andfenestrations in capillary

just holes which allow

movement of dissolved

solutes (NOT large

proteins) into/out

1. Diffusion: O2, CO2,

water, waste products

all can diffuse through

capillary into interstitial fluid

o very good, thin wall and large total cross-sectional area

2. Filtration: fluid moves from capillary out to interstitial space

3. Reabsorption: movement of fluid from interstitial space back



Arteries: larger proportion of elastic tissue allow volatile pressure

changes during heart contraction

Low resistance, little drop in BP – highest BP

Arterioles: smaller but mostly smooth muscle under control of ANS =

vasoconstriction/vasodilation to control blood flow through organs

Thick wall, largest resistance, large drop in BP

Venules: no smooth muscle/elastic tissue blood pressure very low

(lowest), just return blood to veins

Veins: thinner & larger diameter to contain 70% total blood volume

Smooth muscle innervated by ANS for increasing venous

return/EDV, and elastic tissue allows them to expand

Starling Forces

4 different forces that determine whether filtration or reabsorption occurs

Hydrostatic forces:



1. capillary hydrostatic pressure (Pc – Pressure of capillary): normal blood

pressure, forcing blood outwards on the walls of capillaries cause filtration

35 mmHg arterial end; 15 mmHg venous end

2. interstitial-fluid hydrostatic pressure (PIF – Pressure of Interstitial-fluid;

thus out of the capillaries): pressure exerted by interstitial fluid pushingback on capillary cause reabsorption

-6 mmHg (negative interstitial-fluid pressure means it’s lower and

will suck fluid out of capillaries filtration) to 6 mmHg (brain, liver,

kidney: force fluid back into capillaries reabsorption, and

prevents organ swelling)

Osmotic forces: (due to large proteins in plasma/interstitial fluid which can’t

move across/diffuse)

3. osmotic force of plasma proteins (“Pi”p – Pi = osmotic pressure, p =

plasma): proteins concentration inside capillary dissolved in plasma = water

wants to move in reabsorption

28mmHg usually, enough to draw fluid back

4. osmotic force of proteins in interstitial space (“Pi” IF): protein outside

capillaries draw fluid out filtration

but force is low: 3 mmHG – still cause filtration, maybe not net

Net Filtration Pressure (NFP)

if positive net filtration pressure, fluid out of the capillary

o we would be a big bloated mess? Nope, forunateuly there is

lympathatic system to take up excess interstitial fluid!

think of it: add forces for water out, substract forces for water in

(pressure pushing out and pushing in; proteins inside absorbing in

and proteins outside absorbing out)

The Lymphatic System

Large network of capillaries & vessels that return excess fluid/other

dissolved substances in the interstitial spaces back into circulation

Excess fluid passes through the lymphatic capillaries through their

one-ended openings return fluid to larger collecting vessels

pass through lymph nodes which filter fluid send it back to

venous circulation (near heart) through collecting ducts



Edema

Accumulation of fluid in interstitial space causing swelling

Doesn’t occur usually: lymphatic system removes any excess fluid

Occurs when:

o Lifting weights, pinch off veins, increase pressure incapillaries, excess interstitial fluid

o Malnutrition; decreased plasmid proteins, fluid want to move

out & accumulate, bloated abdomen of malnourished children

o Lymphatic system blockage/disruption

When I was in grade 7, my dad walked into a Staples store and found out

line paper was on sale.

8 years later, I still haven’t bought another sheet of paper.

Control and Regulation of Cardiovascular System

Remember!



1. Local control mechanisms in the organs themselves

Autoregulation: most organs & tissues control their own blood flow

Individual capillary beds maintain relatively constant blood flow

despite changes in BP through changing vessel radius (2 theories)

1. Myogenic Theory: occur in brain, heart, and kidneys (delicate organs)

contraction/relaxation of smooth muscle; it’s a reflex that’s built

into the arterioles

sudden increase in BP arterioles momentarily expand smooth

muscle stretch flow too much oh no ! more Ca++ into muscle

cells muscle cells contract and vessels constrict blood flow

after constriction will decrease, so does BP

Opposite occur when blood pressure drop (vasodilation occurs)

2. Metabolic Theory: changing metabolic activity of an organ = change blood

flow to that organ



Exercise muscle uses oxygen & produces CO2, lactic acid, ADP

and heat all of which = cause local vasodilation and increase

blood flow to active tissue

Opposite = when you hyperventilate, too much O2 and too little

CO2, vasoconstriction and decreased blood flow (in brain = passout)

2. Humoral mechanisms: regulation of blood flow by on chemicals in the

blood

vasoconstrictors

epinephrine when binds to ALPHA receptors (on blood vessels in

intestines/kidney) and cause vasoconstriction (recall it also increase

HR and stroke volume)

Angiotensin II (Ang II) most powerful vasoconstrictor; renal

system

Vasopressin (ADH) renal system

Vasodilators

Epinephrine when binds to BETA receptors (on blood vessels in

skeletal/cardiac muscle & liver)

Kinins: family of hormones

Histamine: released from damaged cells (also increases capillaries

permeability together = swelling after injury)

ANF3. Autonomic nervous system (ANS)

Equation comes from: Flow = pressure gradient / resistance

On a whole body level: Cardiac Output = Mean Arterial Pressure / Total

Peripheral Resistance



(Then just rearrange the equation: pressure gradient = flow x resistance)

MAP (mean arterial pressure;BP) = CO x TPR (total peripheral resist.)

So to increase blood pressure, either increase cardiac output (more

blood pumped out) or the resistance of vessels (e.g. more kinks)

The sympathetic nervous system: activated during fight/flight

increase CO (previous module)

as well as TPR release neurotransmitter norepinephrine

general vasoconstriction BP goes up!

o but don’t want to decrease blood flow to muscles, so release

acetylcholine to cause vasodilation there

o effects similar to hormone epinephrine

The parasympathetic nervous system: activated during rest and relaxation

Decreases HR and SV to decrease CO

Decrease TPR too general vasodilation in body (by inhibiting

vasoconstricting effects of SYN) BP goes down!

The Baroreceptor Reflex

Example: stand up suddenly, blood pooled in legs and not returning to heart

immediately (drop in venous return/EDV/CO) and BP/blood flow will drop in

brain – body needs to increase BP, by increase CO/TPR

Drop in BP detected by baroreceptors in the aortic arch and carotid

sinuses (sensor) receptors send fewer AP back to cardiovascular centre in brain stem

(effector) frequency of AP proportional to blood pressure

brain sends signals to

o heart to increase HR/force of contract (hence CO and hence

BP)

o blood vessels (arterioles) to constrict and increase TPR

together BP (controlled variable) returns to 120/80 (set point)

Does the opposite when BP too high



9/15/2012 1:11:00 PM

physiology notes semester 1

Documents