Lecture 4: Physiology of Kidney - ECF Volume Regulation

Question 1

what are the major ECF osmoles?

cause water to be drawn out of the cell

Answer 1

Na+ and Cl-

Question 2

what is the major ICF osmoles?

cause water to be drawn into the cell

Answer 2

K+ salts

Question 3

describe the renal response to a low ECF volume (hypovolaemia)

Answer 3

• increased salt and water loss as in vomiting, diarrhoea or excess sweating > decreased BP > decreased carotid sinus baroreceptor inhibiton of sympathetic discharge.
• increased sympathetic discharge > increased renal arterial constriction > increased renin > increased angiotensin II > increased ECF volume > increased blood pressure.

Question 4

how does angiotensin II increase ECF volume?

Answer 4

• increases Na+ reabsorption from the proximal tubule and therefore less Na+ excreted.
• increases distal tubule Na+ reabsorption and therefore less Na+ excreted.

Question 5

which cells produce the hormone renin?

Answer 5

juxtaglomerular cells (JG)

Question 6

list the factors that control renin release

Answer 6

1. increased renin release when pressure in afferent arteriole at the level of the juxtaglomerular cells decreases. JG cells act as renal baroreceptors.
2. increased sympathetic nerve activity causes increased renin release via beta1 effect.
3. rate of renin secretion is inversely proportional to rate of delivery of NaCl at the macula densa (specialised distal tubule). Decreased NaCl delivery > increased renin.
4. angiontensin II feeds back to inhibit renin.
5. ADH inhibits renin release (osmolarity control).

Question 7

list the reasons why angiotensin II is fundamentally important in the bodys response to hypovolaemia

Answer 7

1. it stimulates aldosterone and therefore NaCl and H2O retention
2. It is a very potent biological vasoconstrictor, 4-8x more potent than NE, therefore contributes to increased total peripheral resistance.
3. it acts on the hypothalamus to stimulate ADH secretion > increased H2O reabsorption from collecting duct.
4. it stimulates the thirst mechanism and the salt appetite (in the hypothalamus).

Question 8

Patients with Conn’s syndrome (primary hyperaldosteronism), are K+ depleted but not hypernatraemic. Why is this?

Answer 8

• aldosterone increases ECF volume > expansion stimulates the release of atrial natriuretic peptide (ANP) from atrial cells which promotes sodium excretion, causing loss of Na+ and H2O i.e. natriueresis