An 83-year-old man visits his doctor for a checkup, and he is found
to have hypertension. The physician wants to
avoid the use of β-blockers and α-blockers
with this patient because of the unpleasant adverse
effects of these medications on the elderly,
so he prescribes an angiotensin-converting enzyme inhibitor instead.
This drug is known to decrease the formation of
angiotensin II in the body.
In addition to increasing aldosterone levels, how else does
directly act?
|
Pharmacology of Renin Angiotensin Aldosterone System
Angiotensinogen from liver - concentration, therefore BP, CONTROLLED BY:
1.Corticosteroids
2.Estrogens
3.Thyroid hormone
4.Pregnancy
5.Angiotensin II
Renin from Juxta Glomerular Apparatus of nephron (granular cells - sensitive to pressure; SNS; K+)
controlled by:
- Na delivery to JGA
- SNS - beta1
- Pressure inc. - stretch activated Ca channel - inhibits AC = decreased renin
- AT 2 - negative feedback control on renin but positive feedback on angiotensinogen
AT2 effects:
- subfornical region of brain (no BBB)
- stimulates thirst
- triggers salt intake
- vasoconstriction - 40x > NE: Gq receptor als0 + rho kinase (dec. MLCP); central effect SNS; resets baroreceptor so no reflex BRADYcardia
- vascular cell growth (remodelling)
- increases aldosterone by stimulating adrenal cortex (zona glomerulosa) = Na and H2O reabsorption = inc. blood volume = inc. BP
Drugs that modulate RAAS
Renin release blockers - β-blockers (propranolol, metoprolol)
Centrally-acting α2 agonists (clonidine)
Renin inhibitors - Aliskiren
ACE inhibitors - Captopril, enalapril
Angiotensin receptor
Blockers (ARBs) -
Losartan
Aldosterone antagonists - Spironolactone, eplerenone
β1-blockers decrease sympathetic-driven increase of renin release
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