First Aid - Renal Physiology III

Question 1

Where are angiotensinogen, Renin, and ACE produced?

Answer 1

Angiotensinogen is produced in the liver. Renin is produced in the kidneys. ACE is produced in the Lungs and kidneys.

Question 2

What are the six sites of action of angiotensin II?

Answer 2

Vascular smooth muscle, efferent arteriole of glomerulus, adrenal gland, posterior pituitary, proximal tubule, hypothalamus

Question 3

How does angiotensin II raise blood pressure?

Answer 3

AngII acts on AT 1 receptors on vascular smooth muscle causing vasoconstriction and elevating blood pressure.

Question 4

How does Angiotensin II act to preserve renal function?

Answer 4

AgII constricts the efferent glomerular arteriole, increasing filtration fraction of GFR in low volume states.

Question 5

How does Angiotensin II act to increase Na+ reabsorption?

Answer 5

AngII acts on the adrenal gland to increase Aldosterone secretion, causing increased Na+ channel and Na+/K+ pump insertion in Principle cells (via mineralocorticoid receptors).

Question 6

How does Angiotensin II act to increase H2O reabsorption?

Answer 6

AngII acts on the posterior pituitary to secrete ADH which then triggers the insertion of aquaporins in the Principle cells of the collecting ducts (via V2 receptors).

Question 7

What effect does angiotensin II have in the Proximal Convoluted Tubule?

Answer 7

AngII increases Na+/H+ exchanger activity in the PCT increasing Na+, HCO3, and H2O reabsorption. May allow “contraction alkalosis”.

Question 8

How does angiotensin II act to increase thirst?

Answer 8

AngII stimulates the hypothalamus to trigger sensation of thirst.

Question 9

What are the primary functions of Angiotensin II?

Answer 9

Affects baroreceptor function, limits reflex bradycardia which would normally accompany its pressor effect. Helps maintain Blood volume and blood pressure.

Question 10

What are the primary functions of ANP (alpha-natriuretic peptide)?

Answer 10

ANP is released by the atria in response to increased volume, may act as a check on renin-angiotensin-aldosterone system; relaxes vascular smooth muscle via cGMP, causing inc GFR, decreased renin.

Question 11

What are the primary functions of ADH?

Answer 11

Primarily regulates osmolarity, also responds to low blood volume states

Question 12

What are the primary functions of Aldosterone?

Answer 12

Primarily regulates ECF Na+ content and volume, responds to low blood volume.

Question 13

What does the juxtaglomerular apparatus consist of?

Answer 13

JG cells (modified smooth muscle of the afferent arteriole) and the macula densa (NaCl sensor, part of the distal convoluted tubule).

Question 14

What do juxtaglomerular cells respond to and what do they secrete?

Answer 14

JG cells secrete Renin in response to decreased renal blood pressure, decreased NaCl delivery to distal tubule, and increased sympathetic tone (B1)

Question 15

How does the juxtaglomerular apparatus defend GFR and medication may affect the JGA?

Answer 15

The JGA defends GFR via renin-angiotensin-aldosterone system. Beta-blockers may decrease BP by inhibiting the B1-receptor of the JGA, causing decreased Renin release.

Question 16

Four major endocrine functions of the kidney

Answer 16

Production of erythropoietin, 1,25-(OH)2 Vitamin D, Renin, and Prostaglandins.

Question 17

What cells produce erythropoietin and in response to what trigger?

Answer 17

Erythropoietin is produced by interstitial cells in the peritubular capillary bed in response to hypoxia.

Question 18

What cells produce 1,25-(OH)2 Vitamin D?

Answer 18

Proximal tubule cells convert 25-OH Vitamin D to 1,25-(OH)2 Vitamin D with 1alpha-hydroxylase (amplified by PTH)

Question 19

What is the production and action of prostaglandins in the kidney? What common drugs interrupt this action?

Answer 19

Paracrine secretion of prostaglandins causes vasodilation of the afferent arterioles to increase RBF. NSAIDs block renal-protective prostaglandin synthesis causing constriction of afferent arterioles and decreasing GFR, possibly inducing acute renal failure.