1. 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
  2. Aldosterone
    • acts on kidney by increasing sodium/potassium exchange
    • promotes retention of sodium + water
    • can also mediate pathologic changes in CV fxn
  3. 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
  4. 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
  5. ARBs
    • cause vasodilation
    • suppress aldosterone
    • promote sodium/water excretion
    • ↓BP
  6. DRI
    • binds tightly w/renin
    • inhibits angiotensinogen-->angioII
    • suppression of entire RAAS
  7. 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
  8. 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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