Urinary System

Chapter 25

Urinary System: Anatomy

Kidneys Ureters Urinary Bladder Urethra Urethral opening

Figure 25.1a

Renal Anatomy

Paired retroperitoneal bean-shaped organs Located in the dorsal upper lumbar region Encased in the renal fat pad

Renal Anatomy: Internal

Superficial: renal cortex Renal medulla: deep to the cortex

Contains medullary pyramids separated by renal columns Medullary pyramids end in the papilla

Renal pelvis: merges with the ureter

Figure 25.3b

Renal Anatomy: Functional Nephron: the functional unit of the kidney

Figure 25.4b

Nephron: Anatomy Bowman’s capsule is continuous with the Proximal convoluted tubule (PCT); cells cuboidal with microvilli Loop of Henle

Descending limb; simple squamous Ascending limb; simple cuboidal to columnar

Distal convoluted tubule; cuboidal Collecting duct; cuboidal

Figure 25.4b

Nephron

Figure 25.5a

Cortical nephrons: located in the renal cortex (about 80%)

Juxtamedullary nephrons: at the cortical-medullary junction with the loop of Henle deep into the medulla

Nephron: Anatomy Afferent arteriole

Glomerulus: fenestrated capillaries

Efferent arteriole Peritubular capillaries

(PCT and DCT) involved in reabsorption

Vasa recta (medullary loop of Henle) involved in forming concentrated urine

Figure 25.5a

Nephron: Anatomy

Afferent arteriole bifurcates to form the - Glomerulus (a capillary bed encased in the glomerular

capsule) which is drained by the - Efferent arteriole

{The only arteriole capillary arteriole sequence in the body}

Figure 25.7a

Nephron: Anatomy

Glomerular (Bowman’s) capsule surrounds the glomerulus Podocytes adhere to the glomerulus (visceral membrane) Spaces between the foot processes of the podocytes form

filtration slits Capsular space surrounded by simple squamous epithelium

(parietal membrane)

Figure 25.7a

Nephron: Anatomy

Filtration membrane; lies between the capillary blood and the capsular space Fenestrated endothelium of the capillaries Visceral membrane of glomerulus (podocytes) Fused basement membranes

Figure 25.7cFigure 25.7a

Nephron: Anatomy

Juxtaglomerular (JG) apparatus DCT in close proximity to the afferent arteriole

JG cells around the afferent arteriole sense blood pressure and produce renin

Macula densa cells in DCT sense flow rate and chemical or osmotic changes in the filtrate

Figure 25.6

Mechanisms of Urine formation

Kidneys filter ~ 180 L of fluid/day Urine production ~ 1.8 L/day

Mechanisms of Urine Formation

Figure 25.8

Urine formation involves three phases Glomerular filtration Tubular reabsorption Tubular secretion

Glomerular Filtration

A passive process due to hydrostatic pressure across the filtration membrane Filtration membrane: extremely permeable to water and

solutes (molecules < 3nm pass freely) Glomerular blood pressure is higher than other capillary

beds (55mm Hg rather than 18mm Hg) Filtrate formed is a protein free filtrate of plasma

Figure 25.9

Glomerular Filtration

Composed of 3 forces: Glomerular hydrostatic pressure (HPg) = glomerular blood pressure

[Blood capsule]

Colloid osmotic pressure (OPg) = osmotic flow toward blood; [Capsule blood]

Capsular hydrostatic pressure (HPc) = pressure exerted by capsular fluid [Capsule blood]

Net Filtration Pressure (NFP)

Figure 25.9

Glomerular Filtration

Net Filtration Pressure (NFP) NFP = HPg – (OPg + HPc)

= 55 – (30 + 15) = 10mm Hg

Figure 25.9

Glomerular Filtration Rate (GFR)

GFR = volume of filtrate formed each minute 3 factors

Total surface area available for filtrationFiltration membrane permeabilityNFP: pressure changes have dramatic impact

on filtrate volume. Normal GFR = 120-125 ml/min

Glomerular Filtration Rate (GFR)

Regulation of GFR: IntrinsicExtrinsic

GFR needs to be held within a narrow range for appropriate reabsorption to occur

Regulation of GFR: Intrinsic

Renal autoregulation: Myogenic mechanism: Afferent arteriole smooth

muscle responds to stretch systemic BP Afferent constriction systemic BP Afferent dilationBoth help to maintain GFR

GFR: Intrinsic

Tubuloglomerular feedback (macula densa) Macula densa cells of Juxtaglomerular (JG) Apparatus

sense filtrate flow rate & osmotic signals [NaCl] Flow or OSM promotes afferent arteriole dilation Flow or OSM promotes afferent arteriole constriction

Figure 25.6

Regulation of GFR: Extrinsic

Extrinsic control: Neural & Hormonal Neural = SNS

Stress shunts blood to vital organs:Norepinephrine causes vasoconstriction of

afferent arterioles & inhibits filtrate formationTriggers renin / angiotensin system

(hormonal)

Regulation of GFR: Extrinsic

Renin / angiotensin system Other factors:

Prostaglandins Nitric OxideAdenosineEndothelinAtrial Natriuretic Peptide

Extrinsic GFR regulation

Renin release: Reduced stretch (i.e. BP) stimulates JG cells to release renin Stimulation of macula densa that cause vasodilation (decreased

flow or decreased OSM) also causes JG cells to release renin Direct stimulation of JG cells by b-adrenergic receptors (SNS)

Figure 25.6

Renin/Angiotensin System

Renin acts on Angiotensin to form Angiotensin I Angiotensin I is converted to Angiotensin II

By Angiotensin Converting Enzyme (ACE) in lung capillary endothelium.

Renin/Angiotensin System

Angiotensin II: actions Vasoconstrictor: systemic BP Enhances Na+ reabsorption in PCT (Proximal

Convoluted Tube) Stimulates the adrenal cortex to release aldosterone

causing renal tubule reabsorption of Na+

Renin/Angiotensin System Angiotensin II: actions

Vasoconstriction of efferent arteriole is greater than afferent resulting in HPg which helps to maintain GFR near normal

Causes mesangial cells to reduce surface area of glomerular capillaries which GFR

Stimulates thirst centers

Regulation of GFR: Extrinsic

Other factors: Prostaglandins (PGE2, PGI2) vasodilators in response to SNS &

angiotensin II: oppose effects of norepinephrine and angiotensin II

Nitric Oxide: vasodilator from vascular endothelium Adenosine: systemic vasodilator but acts to constrict renal

vasculature Endothelin: vasoconstrictor from vascular endothelium Atrial Natriuretic Peptide (ANP)

Responds to BP to inhibit Renin/Angiotensin system

Figure 25.10

Tubular Reabsorption

Every 45 min the entire blood plasma volume is filtered by the kidneys.

Most tubular contents are reclaimed (reabsorbed).

Routes of Water and Solute Reabsorption

Three membrane barriers Luminal membrane Basolateral membrane Endothelial membrane

Figure 25.11

Routes of Water and Solute Reabsorption Na+ Reabsorption:

Diffuses into tubular cell (co-transport) Luminal membrane

Actively transported to interstitial fluid Basolateral membrane

Diffusion through endothelium Endothelial membrane

Na+ reabsorption provides reabsorption provides energy & mechanisms energy & mechanisms for reabsorbing most for reabsorbing most other solutesother solutes

Figure 25.12

Reabsorption of water / ions / nutrients

Passive tubular reabsorption: Na+ ions establish an electro-chemical gradient

favoring anions (Cl- & HCO3-)

Na+ establishes an osmotic gradient allowing water (via aquaporins) to leave water permeable region (PCT & Loop)

As water leaves the tubules the remaining solutes become more concentrated & follow their diffusion gradient out of the filtrate (cations, fatty acids, urea)

Reabsorption of water / ions / nutrients

Secondary active transport: Na+ moves down its diffusion gradient in co-transport with

specific substances (glucose, amino acids, lactate, vitamins, most cations)

Transport maximum for various solutes is dependent upon the number of carriers for Na+ co-transport

Plasma proteins: endocytosed & hydrolyzed to amino acids

Non-Reabsorbed Substances

Non-reabsorption due to: Lack of carriers Lipid insolubility Molecules too large to pass through membrane pores

Non-reabsorbed substances are usually nitrogenous wastes Urea (50-60% reclaimed) Creatinine: not reabsorbed

Proximal Convoluted Tubule (PCT); Reabsorption

Figure 25.4b

PCT is the most active in reabsorption: All glucose, lactate, & amino acids Most Na+, H2O, HCO3

- , CL- and K+

65% Na+ and H2O 90% HCO3

-

50% CL-

55% K+

Table 25.1 Summary of Tubular Reabsorption

Loop of Henle; Reabsorption

Figure 25.4b

Descending limb: H2O reabsorbed by osmosis

Ascending limb: Na+, Cl-, K+ active transport Ca2+, Mg2+ passive transport

Distal Convoluted Tubule; Reabsorption

Figure 25.4b

Na+ : Aldosterone mediated Ca2+ : PTH mediated Cl- : diffusion H2O : osmosis

Collecting Duct; Reabsorption Most reabsorption in collecting duct due to hormonal

influencesNa+ : Aldosterone vs ANPHCO3

-, H+, K+, Cl- : passive transport & co-transport

H2O : ADH dependentUrea: facilitated diffusion

Tubular Secretion Tubules also secrete substances into the filtrate. H+, K+, NH4

+, creatinine & organic acids Important functions:

Disposes of substances not in original filtrate (certain drugs)

Replaces substances in filtrate that were reabsorbed (urea/uric acid)

Disposes of excess K+

Controls pH (Ch. 26)

Urine consists of filtered & secreted substances

Tubular Secretion

Figure 25.4b

Important functions: Disposes of substances not in the original filtrate (certain drugs) Replaces elements in filtrate that were reabsorbed (urea/uric acid) Disposes of excess K+

Controls pH (Ch. 26)

Urine consists of filtered & secreted substances

Regulation of Urine Concentration and Volume Body fluids kept @ ~ 300 mOsm (milliosmoles) Counter current multiplier:

Interaction between the filtrate in the juxtamedullary Loop of Henle & blood flow in vasa recta.

Regulation of Urine Concentration

Figure 25.13

Figure 25.14

Figure 25.5a

Osmotic Gradient in the Renal Medulla

Capillary Beds

Loop of Henle: Countercurrent Mechanism

Counter Current Multiplier Descending loop:

freely permeable to H2O impermeable to solutes

H2O leaves filtrate by osmosis

Filtrate becomes highly concentrated to 1200 mOsm at deepest portion of loop

Figure 25.14

Counter Current Multiplier Ascending Loop

impermeable to H2O permeable to NaCl

Most NaCl re-absorption occurs in ascending thick segment

Filtrate becomes more dilute as it ascends (100 mOsm)

Interstitial fluid develops a concentration gradient that is maintained by the movement of H2O and NaCl.

Figure 25.14

Counter Current Multiplier Medullary Collecting Ducts are

permeable to urea Urea diffuses into interstitium

Urea makes a large contribution to the increased interstitial osmolality

Figure 25.14

Vasa Recta: Counter Current Exchanger Slow blood flow Freely permeable to H2O & NaCl As blood descends it loses H2O &

gains NaCl As blood ascends into cortex it gains

H2O & loses NaCl Protects medullary gradient by

preventing rapid removal of salt

Figure 25.14

Loop of Henle: Countercurrent Mechanism

Figure 25.14

Regulation of Urine Concentration and Volume Dilute urine: reaches the end

of Ascending Loop Production of dilute urine

requires nothing further Absence of ADH

Regulation of Urine Concentration and Volume

Concentrated urine: ADH dependent reabsorption

of H2O from collecting ducts ADH induces production of

aquaporin complexes in collecting duct

Formation of Dilute and Concentrated Urine

Figure 25.15a, b

Regulation of Urine Concentration and Volume

Diuretics: Osmotic (retains H2O in filtrate) Inhibition of ADH Inhibition of Na+ reabsorption

Urine Physical Characteristics:

Clear/yellow Slight aroma develops ammonia on standing pH: usually ~ 6.0 (range 4.0-8.0) Specific gravity: 1.001-1.035

Chemical Composition: 95% H2O 5% Solutes: mostly urea, uric acid & creatinine

Ureters

Tri-layered: Mucosa Muscularis Adventitia

Moves urine by peristalsis

Figure 25.18a, b

Urinary Bladder

Tri-layered: Mucosa: transitional epithelium Muscularis: Detrusor muscle Adventitia: except superior portion – which has a

peritoneal covering Capacity: 800-1000ml

Figure 25.18a, b

Urinary Bladder

Figure 25.18a, b

Urethra

Thin walled muscular tube Internal urethral sphincter: involuntary External urethral sphincter: voluntary

Figure 25.18a, b

Urethra

Females: short urethra external urethral orifice Males: prostatic urethra membranous urethra

penile urethra external urethral orifice

Figure 25.18a, b

Urine Storage

Figure 25.20a

Storage reflex: As bladder fills a sympathetic spinal

cord reflex causes; Contraction of internal & external

urethral sphincters Inhibition of contraction of

detrusor muscle

Micturition (Voiding or Urination)

Figure 25.20b

Voiding: Activation by visceral afferent fibers Stimulates Pontine Micturation center which then: Stimulates contraction of detrusor muscle Inhibits contraction of internal sphincter Inhibits sympathetic & somatic fibers allowing

relaxation of external sphincter

Voluntary contraction of external sphincter can postpone voiding