lecture 7 - targets & RAAS

Question 1

role of RAAS

Answer 1

• works synergistically with SNS
• critical for controlling BP
• alters vascular tone & controls natriuresis
• activation results in decreased space for blood to exist in and increased BV

Question 2

what causes a release of renin

Answer 2

released in response to sympathetic stimulation

Question 3

drugs targeting the RAAS

Answer 3

• ACE inhibitors
• angiotensin receptor antagonists (ARBs)
• aldosterone antagonists
• calcium channel blockers
• diuretics
• beta-blockers

Question 4

describe ACE-Is and adverse effects

Answer 4

example: cilazipril
- decreases angiotensin 2 levels
- increases bradykinin (vasodilation)

adverse effects

1. dry cough
2. angioedema (abnormal swelling & inflammation)

Question 5

angiotensin receptor blockers/antagonists (ARBs)

Answer 5

competitive antagonists at AT-1 receptors

blocks activity of RAAS

e.g. losartan

Question 6

ACE-Is, ARB or both?

Answer 6

both decrease likelihood of an adverse cardiovascular event

ACE-Is generally more effective, but more likely to have adverse effects

ARBs possible as substitute

combination can be dangerous, increased risk of hyperkalemia and AKI

Question 7

aldosterone antagonists

Answer 7

e.g. spirolactone

antagonists at mineralocorticoid receptor

inhibits Na+ reabsorption caused by aldosterone

Question 8

calcium channel blockers

Answer 8

Ca2+ channels are important in muscle excitation & contraction

blockers inhibit SM contraction

• decrease vasoconstriction
• decrease BP

e.g. varapamil, nifedipine

Question 9

diuretics

Answer 9

oppose the retention of water and Na+

increases excretion of Na+

amiloride counteracts RAAS activity, as does thiazide

Question 10

beta blockers

Answer 10

main action of SNS, therefore affecting RAAS

competitive antagonists at B-adrenergic receptors

decreases cardiac contractility, decreases renin release

e.g. metoprolol