Regulation of Osmolarity

Question 1

What are the components of the RAAS?

Answer 1

1. Renin – Released in response to a decrease in pressure in afferent arterioles at the level of the juxtaglomerular cells. In a way, the JG cells behave like ‘renal baroreceptors’, when there is less distension there is more renin released.
2. Angiotensinogen – Is converted by renin to form angiotensin I. Angiotensin I is then converted into Angiotensin II by angiotensin-converting enzyme (ACE) which is found in the lungs. Angiotensin II is a potent vasoconstrictor peptide which causes blood vessels to narrow resulting in increased blood pressure. Angiotensin II also stimulates the secretion of aldosterone from adrenal cortex.
3. Aldosterone – Causes renal tubules to increase their reabsorption of Na and H2O into the blood, thereby increasing ECF in the body and therefore increasing BP.

Question 2

What are the effects of Angiotensin II?

Answer 2

1. An increase in aldosterone levels via secretion from the adrenal glands
2. A decrease in peritubular hydrostatic P, which allows for an increase in Na+ reabsorption.
3. Increases blood pressure via vasoconstriction
4. Activates the hypothalamus to produce ADH
5. Stimulates the sympathetic system

Question 3

What are the renal responses to hypovolaemia?

Answer 3

1. Increased NaCl and H2O loss leading to:
   
   1. Decreased perfusing volume
   2. Decreased venous pressure
   3. Decreased venous return
   4. Decreased atrial pressure
   5. Decreased end diastolic volume
   6. Decreased Stroke volume
   7. Decreased cardiac output
   8. Decreased BP
   9. Decreased carotid sinus baroreceptor inhibition of sympathetic discharge
2. Increased sympathetic discharge
   
   1. Leads to venous constriction
   2. Which leads to increased total peripheral resistance
   3. Which brings BP back to normal.