Lecture 7: RAAS

Question 1

RAAS achieves 2 main processes?

Answer 1

1. Alteration of vascular tone
2. controlling natriuresis

released in response to SNS acts via AT1 receptors activating phospholipase C and causing Ca²⁺ release causing SM contraction

Question 2

Beyond Angiotensin II?

Answer 2

can be cleaved to Angiotnesin III and IV

III = promotes aldosterone secretion

IV = binds own receptors causing effects including inhibition of clot clearance by promoting release of plasminogen activating inhibitor 1

Question 3

Aldosterone

Answer 3

• released due to Ang 2 and 3 (AT1 receptor activation) as well as high K⁺
• inc Na²⁺ reabsorption and thus water

Question 4

ACE inhibitors

Answer 4

eg. cilazipril

Mimic angiotensin I

also ACE = kininase II so they degrade bradykinin causing a dry cough (common) and angioedema (uncommon swelling of lips and airways and is dangerous)

Question 5

ARBs

Answer 5

• compeditive antagonist at AT-1
• blocks most of RAAS
• eg losartan

Question 6

ARB and ACE-i together?

Answer 6

nah don’t do it aye

shown to increase risk of hyperkalaemia and acute kidney injury. You’ll be more fucked than Tommy Hayes at Kegs and Pong

Question 7

Aldosterone antagonists

Answer 7

sprionolactone is an antagonist for the Mineralocorticoid receptor

Question 8

beta blockers?

Answer 8

eg. Metoprolol

compeditive antagonist at B-adrenergic receptors, primarily B1

decrease cardiac contractilitym decrease renin secretion