4.4A. Control of body fluid volumes and extracellular fluid osmolality.

Question 1

I. Renin-angiotensin-aldosterone system (RAS/RAAS)
1. How is Renin-angiotensin-aldosterone system (RAS/RAAS) activated?

Answer 1

This system gets activated by a decrease in arterial pressure – acts to increase arterial pressure (Pa) by increasing blood volume.

Question 2

I. Renin-angiotensin-aldosterone system (RAS/RAAS)
2. How does Renin-angiotensin-aldosterone system (RAS/RAAS) work?

Answer 2

It is a slower system for blood pressure/volume regulation than the baroreceptor reflex, because it is hormonal, rather than neural
1. Decreased Pa is sensed by afferent arteriole mechanoreceptors which trigger a conversion of prorenin to renin by the juxtaglomerular cells, which then secrete renin
- Renin is synthesized in the renal granular cell
2. Renin catalyzes the conversion of (plasma) angiotensinogen to angiotensin I
- Angiotensinogen is synthesized in the liver
3. Angiotensin I is converted via angiotensin-converting enzyme (ACE) to angiotensin II
- ACE is present in the lungs and the kidneys

Question 3

I. Renin-angiotensin-aldosterone system (RAS/RAAS) - Angiotensin II stimulates several processes
3A. What are the 4 processes that ANGII stimulate?

Answer 3

1. Aldosterone synthesis in the adrenal cortex (zona glomerulosa)
2. Enhanced Na+-H+ exchange
3. Thirst centers + ADH secretion in the hypothalamus and pituitary gland
4. Vasoconstriction of systemic vessels

Question 4

I. Renin-angiotensin-aldosterone system (RAS/RAAS) - Angiotensin II stimulates several processes
3B. How does ANGII enhance Na+-H+ exchange

Answer 4

ANGII promotes Na+-reabsorption in the PT, TAL, early DCT

Question 5

I. Renin-angiotensin-aldosterone system (RAS/RAAS)
3C. How does ANGII promote Vasoconstriction of systemic vessels?

Answer 5

1. ANGII constricts the efferent arteriole in the nephrons = ↑GFR
2. ANGII binds to Gq-coupled receptors on
   VSMCs -> PIP2 -> DAG + IP3 -> ↑[Ca2+] -> ↑TPR

Question 6

I. Renin-angiotensin-aldosterone system (RAS/RAAS)
4. How does aldosterone effect BP?

Answer 6

Aldosterone effects BP via fluid volume, by increasing ENaC expression on principal cells of the distal tubule / collecting duct, to increase Na+-reabsorption

Question 7

II. Atrial natriuretic peptide (ANP)
1. How does Atrial natriuretic peptide (ANP) work?

Answer 7

Released in response to stretching of the atrial walls (as a result of increased BP / volume), ANP opposes many of the effects of aldosterone and ANGII.
-> It acts mostly on guanylyl cyclase-coupled receptors to increase intracellular cGMP and phosphorylation of proteins via PKG

Question 8

II. Atrial natriuretic peptide (ANP)
2. What are the 2 effects of Atrial natriuretic peptide (ANP)?

Answer 8

1. Renal effect
2. Vascular effect

Question 9

II. Atrial natriuretic peptide (ANP)
3. Explain renal effects of ANP

Answer 9

• Dilates afferent arterioles and constrict efferent arterioles to increase GFR
• Decreases Na+-reabsorption (↑Na+-secretion) in the distal tubule by inhibiting ENaCs (via cGMP -> PKG -> ENaC phosphorylation)
• Inhibits renin secretion from juxtaglomerular cells

Question 10

II. Atrial natriuretic peptide (ANP)
4. Explain Vascular effect of ANP

Answer 10

• Dilates arterioles (via cGMP increase in SM)

Question 11

II. Atrial natriuretic peptide (ANP)
5. What are the main consequences of renal and vascular effects of ANP?

Answer 11

the main consequence of its effect is the decrease of blood volume via increased urine production and sodium excretion (natriuresis), which results in decreased blood pressure

Question 12

III. Regulation of body fluids
1. How does Regulation of body fluids occur?

Answer 12

Fluid compartments within the body: There are 3 major fluid compartments:
1) Intravascular compartment: fluid contained within blood and lymphatic vessels - Blood can be subdivided into corpuscular (cell)
and plasma (fluid) components
2) Interstitial (EC) compartment: fluid surrounding the cells

3) Intracellular (IC) compartment: within a cell (includes corpuscular component in the intravascular fluid)