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15 Cards in this Set

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RAAS actions
Angiotensinogen (liver) converted by Renin (kidney) to Ang I which is converted to Ang II by ACE (also by chymase).
AT1 receptor effects
Na and fluid retention
Vasoconstriction
Symp activation
cell growth
Aldosterone secretion

Overall, Increase Pressor response.

Rapidly via increase in Afterload.

Slowly via increasing preload via volume increase.

Also, increase growth factor, synthesizing effects etc, resulting in HYPERTROPHY.
AT2 receptor effects
opposite of AT1.

vasodilation
cell growth inhibition and apoptosis.
Antagonize AT1 receptor.
Aldosterone Mineralocorticoid receptor activation causes?
Na and H2O reabsorption

K and H excretion.
A little about Ang I
It can be chopped up into many active hormones including Ang II etc.
Drugs acting on RAAS
ACE inhibitors: captopril, enalapril

ARBs (AT1-R blocker): Losartan

MR antagonist: spironalactone, eplerenone.
ACE inhibitor drugs
captopril, enalapril (-pril drugs)

Prevents formation of Ang II, prevent breakdown of bradykinin
ACE-i uses
Hypertension: lowers afterload, and preload
(less effective in blacks)

CHF: lowers preload and afterload

done via arterial and venous dilation.

slows progression of diabetic nephropathy.
ACE-i contrainidcations
renal artery stenosis

elevated serum potassium

symptomatic hypotension

PREGNANCY.

side effects: hypotension, chronic non-productive cough(due to increase bradykinin), dysgeusia
ACE-i drug interractions
effect reduced by ibuprofen (NSAID) and enhanced by thiazide or loop diuretics.

reduces digoxin clearance

hyperkalemia with K supplements or K sparring diuretics.
Ang-R blocker (AT1-r blocker): Losartan
Losartan antagonist to AT1R and interferes with AngII from binding its receptor.

NO EFFECT on bradykinin breakdown, so NO COUGH or angioedema.

Indicated for HTN in pts with high or normal renin (NOT in low renin pt due to lack of bradykinin enhancement).//

Indications: HTN, CHF, post MI, post stroke (reduction in events, morbidity and mortality).
Aldosterone action
secretion affected by: Angiotensin II (most potent), plasma potassium levels, ACTH.

Kideny: stimulate sodium retention by distal nephrons, potassium excretion, vol expansion and BP elevation

Other sites: increase BP by CNS mech, stim myocardial fibrosis, reduce arterial elasticity and increase inflammation.
Ald antagonist: Spironolactone
K sparing diuretics, ald-r antagonist, wk antiadrogenic and prog-r agonist.

indication: HTN, CHF (low dose) especially in class III and IV pts.

side effects: gynecomastia, impotence, menstrual irregularities (due to prog and antiadrogenic side effects).
Ald antagonist: Eplerenone
selective ald-r antagonist, also K sparing.

No prog, antiadrogenic effects unlike spironolactone.
Ald Antag: Contrainidcation
hyperkalemia, cirrhosis

Rx interraction: Digitalis clearance affected.