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15 Cards in this Set
- Front
- Back
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RAAS actions
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Angiotensinogen (liver) converted by Renin (kidney) to Ang I which is converted to Ang II by ACE (also by chymase).
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AT1 receptor effects
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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. |
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AT2 receptor effects
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opposite of AT1.
vasodilation cell growth inhibition and apoptosis. Antagonize AT1 receptor. |
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Aldosterone Mineralocorticoid receptor activation causes?
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Na and H2O reabsorption
K and H excretion. |
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A little about Ang I
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It can be chopped up into many active hormones including Ang II etc.
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Drugs acting on RAAS
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ACE inhibitors: captopril, enalapril
ARBs (AT1-R blocker): Losartan MR antagonist: spironalactone, eplerenone. |
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ACE inhibitor drugs
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captopril, enalapril (-pril drugs)
Prevents formation of Ang II, prevent breakdown of bradykinin |
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ACE-i uses
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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. |
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ACE-i contrainidcations
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renal artery stenosis
elevated serum potassium symptomatic hypotension PREGNANCY. side effects: hypotension, chronic non-productive cough(due to increase bradykinin), dysgeusia |
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ACE-i drug interractions
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effect reduced by ibuprofen (NSAID) and enhanced by thiazide or loop diuretics.
reduces digoxin clearance hyperkalemia with K supplements or K sparring diuretics. |
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Ang-R blocker (AT1-r blocker): Losartan
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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). |
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Aldosterone action
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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. |
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Ald antagonist: Spironolactone
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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). |
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Ald antagonist: Eplerenone
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selective ald-r antagonist, also K sparing.
No prog, antiadrogenic effects unlike spironolactone. |
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Ald Antag: Contrainidcation
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hyperkalemia, cirrhosis
Rx interraction: Digitalis clearance affected. |
