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Angiotensin II
- produced in blood and carried to target tissue
- can also be produced locally by individual tissues
- high biological activity
- formed from renin and ACE enzymes
- causes vasoconstriction (primarily arterioles)
- causes release of aldosterone
- can promote pathologic changes in heart and blood vessels
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Aldosterone
- acts on kidney by increasing sodium/potassium exchange
- promotes retention of sodium + water
- can also mediate pathologic changes in CV fxn
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RAAS
- raises BP by causing vasoconstriction and increased blood volume (renal retention of water)
- regulation of BP, blood volume, F/E balance, mediation of certain pathologic Δs associated w/HTN, HF, MI
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ACE Inhibitor
- decrease production of Angio II
- vasodilation, ↓blood volume, prevent/reverse pathologic Δ
- treats pt's w/ HTN, HF, MI, nephropathy
- prevents MI, stroke, death from CVD
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ARBs
- cause vasodilation
- suppress aldosterone
- promote sodium/water excretion
- ↓BP
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DRI
- binds tightly w/renin
- inhibits angiotensinogen-->angioII
- suppression of entire RAAS
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Aldosterone Antagonist
- block receptors for aldosterone
- promote renal excretion of sodium/water (thus ↓BP/volume)
- prevent/reverse pathologic fx of aldosterone on CV structure/fxn
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Explain the process of Aldosterone:
AngiotensinII stimulates the adrenal cortex to release aldosterone, which acts on the distal tubules of the kidney to retain sodium/water and excrete potassium/hydrogen, thus increasing blood volume and blood pressure and maybe CV fx
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