chapter 4-adrenal glands
DESCRIPTION
Chapter 4-Adrenal Glands. Ch. 4-- Study Guide. Critically read (1) pages pp. 61-69 before postsecretory metabolism of adrenal cortical hormones section; (2) pp. 71-76 (physiology of the mineralocorticoids) before Effects on water balance subsection. - PowerPoint PPT PresentationTRANSCRIPT
![Page 1: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/1.jpg)
Chapter 4-Adrenal Glands
4-1
![Page 2: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/2.jpg)
Ch. 4-- Study Guide
1. Critically read (1) pages pp. 61-69 before postsecretory metabolism of adrenal cortical hormones section; (2) pp. 71-76 (physiology of the mineralocorticoids) before Effects on water balance subsection.
2. Comprehend Terminology (the text in bold/italic)
3. Study and understand the text and corresponding figures.
4-2
![Page 3: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/3.jpg)
4.1. Introduction
4-3
![Page 4: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/4.jpg)
§ Introduction1. Adrenal hormones:
– required for maintenance of life– Without them, deranged
electrolyte or CHO metabolism, hypoglycemic coma, and death
– Outer cortex– three steroid hormones: mineralocorticoids, glucocorticoids, and androgens
– Inner medulla—a component of the sympathetic nervous system
4-4
![Page 5: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/5.jpg)
4.2. Morphology
4-5
![Page 6: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/6.jpg)
§ Morphology (1)– Fig. x + 4.11. Location— right above the kidneys
2. Gross Anatomy and Histology–
A. Outer cortex-- > 3/4 of adrenal mass– Divided into 3 zones and produces
steroids;– Zona glomerulosa– aldosterone– Zona fasciculata– cortisol and androgens– Zona reticularis– cortisol and androgens
B. Inner medulla -- @ 1/4 – A modified sympathetic ganglion, releases
epinephrine and norepinephrine4-6
![Page 7: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/7.jpg)
4-7
![Page 8: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/8.jpg)
4-8
![Page 9: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/9.jpg)
4.3. Adrenal cortex
4-9
![Page 10: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/10.jpg)
§ Adrenal Cortex1. Adrenal cortex is essential for maintenance of
life.
2. Addison’s disease– pathological destruction or surgical removal of the adrenal cortex– death within 1-2 weeks
3. Why? 3 categories of hormones: Fig. 4.2– ALL come from cholesterol
– Mineralocorticoids– essential to maintain sodium and potassium balance– Aldosterone + deoxycorticosterone (DOC)
– Glucocorticoids– include cortisol and corticosterone– maintain CHO reserves
– Androgens– on puberty and fetal life4-10
![Page 11: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/11.jpg)
The principal adrenal steroid hormones
4-11
![Page 12: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/12.jpg)
4.3A. Adrenocortical hormones
4-12
![Page 13: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/13.jpg)
§ adrenocortical hormones1. All the adrenal steroids are from
cholesterol– same as other steroids including . . .
2. Naming steroids—– Fully saturated 21-carbon molecule is
called pregnane– Delta– location of double bond(s) and
-ane changes to -ene or to –diene– Presence of a hydroxyl group (-ol)– Presence of a keto group (-one)– Fig. 4.3
4-13
![Page 14: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/14.jpg)
All three reactions are catalyzed by a single enzyme, cytochrome P450SCC. Pregnenolone– an important molecule for other adrenal hormones
4-14
![Page 15: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/15.jpg)
§ Adrenal Cortex (1)1. Pregnenolone and progesterone (21
Carbons) is the common precursor of all steroid hormones produced by the adrenals or the gonads (Fig. 4.4)
4-15
![Page 16: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/16.jpg)
Z. glomerulosa
Z. fasciculata
Z. reticularis; 19 carbons
Z. glomerulosa & reticularis Biosynthesis of adrenal cortical H.
4-16
![Page 17: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/17.jpg)
§ Adrenal Cortex (2)2. A hydroxyl group at carbon 11 is found in
all glucocorticoids–that is corticosterone and cortisol
3. Corticosterone is the major glucocorticoid in the rat but is of only secondary importance in humans
4. Cortisol is the most potent of the naturally occurring glucocorticoids in humans
5. Corticosterone is a precursor of aldosterone (a major mineralocorticoid)
Fig. 4.44-17
![Page 18: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/18.jpg)
Z. glomerulosa
Z. fasciculata
Z. reticularis; 19 carbons
Z. glomerulosa & reticularis Biosynthesis of adrenal cortical H.
Glucocorticoids
A major mineralocorticoid4-18
![Page 19: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/19.jpg)
§ Adrenal Cortex (3)6. Male hormones--Steroids in the 19-carbon
series usually have androgenic (male hormone) activity)
7. Locations--This above reaction normally occurs only after puberty, and is confined to the cells of the zona reticularis (Fig. 4.4)
8. Female hormones--19-carbon steroids are precursors of the estrogens (female hormones; 18-carbon)—unsaturated A ring due to aromatization (loss of the methyl carbon at position 19). This reaction happens in ovary and placenta normally.
Fig. 4.5 4-19
![Page 20: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/20.jpg)
Z. glomerulosa
Z. fasciculata
Z. reticularis; 19 carbons– Male steroid hormones
Z. glomerulosa & reticularis Biosynthesis of adrenal cortical H.
Glucocorticoids
A major mineralocorticoid4-20
![Page 21: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/21.jpg)
Principal 18-carbon estrogens
A
4-21
![Page 22: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/22.jpg)
4.3B. Control of adrenal cortical hormone synthesis
4-22
![Page 23: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/23.jpg)
§ Effects of ACTH1. ACTH has impact on z. fasciculata and
reticularis but not glomerulosa
2. Through G-protein-coupled mem receptor
3. Increases cholesterol availability– in the cell and specifically also in mitochondria
4. (specifically on androgens)--ACTH is the only hormone known to control synthesis of the adrenal androgens (dehydroepiandrosterone sulfate; DHEAS)
5. Adrenarche– Beginning of increased secretion of adrenal hormones at puberty (another similar term: menarche)
Fig. 4.6 + 4.7 4-23
![Page 24: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/24.jpg)
Steroid synthesis by ACTH in Z. Fasciculata
4-24
![Page 25: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/25.jpg)
4-25
![Page 26: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/26.jpg)
§ control of aldosterone synthesis1. Location– in zona glomerulosa
2. ACTH is NOT an important regulator of aldosterone production in most species
3. Angiotensin II (from Angiotensinogen, from liver) regulates the production of aldosterone
How?
4. (first messenger-receptor)—Angiotensin II binds with specific G-protein-coupled receptor
5. (second messengers)– IP3 and calcium to promote the formation of pregnenolone from cholesterol
Fig. x + 4.84-26
![Page 27: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/27.jpg)
4-27
![Page 28: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/28.jpg)
4-28
Angiotensin II
![Page 29: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/29.jpg)
§ control of aldosterone synthesis• Impact by three ions--
6. (K+)-- Cells of the zona glomerulosa are very sensitive to changes in potassium in the ECF; increased K+ (ECF) stimulates production of aldosterone
7. (Na+)-- Aldosterone is the principal regulator of body sodium content
8. (Ca+2)-- Intracellular calcium also stimulates the synthesis of aldosterone.
4-29
![Page 30: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/30.jpg)
4.3C. Adrenal steroid hormones in blood
4-30
![Page 31: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/31.jpg)
§ plasma binding proteins1. CBG, corticosteroid binding globulin (or
called transcortin), and albumin
2. Both are produced in the liver
3. CBG has a single steroid hormone binding site whose affinity for cortisol is 20 times higher than for aldosterone
4. About 95% of the cortisol and about 60% of the aldosterone in blood are bound to protein
4-31
![Page 32: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/32.jpg)
4.4A. Physiology of the mineralocorticoids (Mainly aldosterone & deoxycorticosterone, also others; See Fig. 4.2)
4-32
![Page 33: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/33.jpg)
The principal adrenal steroid hormones
4-33
![Page 34: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/34.jpg)
§ Introduction1. Aldosterone is the most important
mineralocorticoid
2. Aldosterone’s physiology and life-threatening changes:
A. Reabsorption of sodium is decreased and fall of sodium in blood (hyponatremia)
B. An accompanying loss of water
C. Resulting decrease in blood volume called hypovolemia.
D. Locations of these effects– the kidney is the most important; also in the sweat glands, the colon, and the salivary glands
4-34
![Page 35: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/35.jpg)
§ Aldosterone on the kidney-A
1. Increased potassium excretion
2. Sodium retention (decrease in urinary sodium)– The above two ions are not tightly coupled and sodium is not simply exchanged for potassium
3. Increase in body weight due to fluid retention
Fig. 4.13
4-35
![Page 36: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/36.jpg)
4-36
![Page 37: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/37.jpg)
§ Aldosterone on the kidney-B1. Aldosterone sensitive cells called
principal cells found in the nephrons– specifically in the connecting tubule and the cortical portion of the collecting duct
2. Details—– Sodium (two-step transfer)– (A) enters the
principal cells via sodium channels; (B) and is pumped out by sodium-potassium ATPase
– Potassium– ROMK (renal outer medullary K+) channels on both sides of principal cells
– Fig. 9.2; Fig. 4.144-37
![Page 38: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/38.jpg)
4-38
![Page 39: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/39.jpg)
In principal cells of cortical
colleting duct
lumenInterstitium
4-39
![Page 40: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/40.jpg)
§ Aldosterone on the kidney-C1. On principal cells–
A. after 30 minutes– resulting in prolonged half-life of ENaC
B. Later effects--Mainly by increasing the expression of proteins associated of sodium transport
– Fig. 4.14B & 4.14C
4-40
![Page 41: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/41.jpg)
In principal cells—aldosterone effects after 30
min. delay
SGK1– serum glucocorticoid dependent kinase 1ENaC--Epithelial sodium channel
Mainly by prolonging the half-life of ENaC
4-41
![Page 42: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/42.jpg)
In principal cells– later effects of
aldosterone
Mainly by increasing the expression of proteins associated of sodium transport.
4-42
![Page 43: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/43.jpg)
§ Aldosterone on the kidney-D1. Aldosterone also targets intercalated
cells found in the nephrons– specifically in the distal nephron and collecting duct
– Fig. 9.2; Fig. 4.14D
4-43
![Page 44: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/44.jpg)
4-44
![Page 45: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/45.jpg)
Mainly by promoting the secretion of protons (hydrogenions) in luminal membranes
AR– Aldosterone receptors on the cell surface
4-45
![Page 46: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/46.jpg)
4.4B– Regulation of aldosterone secretion
4-46
![Page 47: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/47.jpg)
§ Aldosterone secretion and function1. Stimuli for aldosterone secretion:
– Primary-- Angiotensin II– Also by ACTH and high conc. of potassium
2. Angiotensin II is regulated by renin from the kidney (glomerular arterioles)
– Principal stimulus for renin secretion is a decrease in the blood (or vascular) volume
3. Principal physiology of aldosterone:– Defend the blood volume by reabsorbing
sodium & water from the kidney– X + Fig. 4.15
4-47
![Page 48: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/48.jpg)
4-48
![Page 49: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/49.jpg)
Monitored variables– A--blood volume
B--plasma potassium conc.
4-49
![Page 50: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/50.jpg)
4.5– Physiology of the glucocorticoids
4-50
![Page 51: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/51.jpg)
§ Glucocorticoids1. Physiology roles can be summarized as
“Coping with adversity”
2. Major role-- in maintaining carbohydrate reserves
3. Do have many other functions (Table 4.2); every tissue of the body is affected by glucocorticoids
4-51
![Page 52: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/52.jpg)
§ Major effects on energy metabolism by the glucocorticoids (cortisol etc.)
1. CHO—A. Decrease utilization of glucose
B. Promote hepatic gluconeogenesis (produce sugar from nonglucose precursors)
C. Defend against hypoglycemia
D. Promote glycogen storage in liver and muscle
2. Proteins--Inhibit protein synthesis and promote proteolysis (rapid breakdown of stored protein in muscle tissues etc.)
3. Lipids-- Increase lipolysis in adipose tissue
Fig. 4.16 4-52
![Page 53: Chapter 4-Adrenal Glands](https://reader036.vdocuments.net/reader036/viewer/2022081513/56813ecb550346895da935e1/html5/thumbnails/53.jpg)
4-53