acts on DCT to downreg Na/Cl transported and decrease Na reabsorption
blocks Na transport from ascending loop of henle to interstitium
in NL LV fx, lower BP with little effect on CO by inhibiting angII mediated vasoconstriction, Na retention and SYMP activity, as well as lowering aldosterone levels to lower volume
block angII effects, but don't get bradykinin effect
block SYMP outflow to heart, blood vessels and kidney
block vasoconstriction from norepi and epi
arteriolar dilation, leads to decreased afterload
arteriolar and venodilator, highly potent and rapid action make it ideal for HTN emergencies
smooth muscle relaxation mediated by PDE inhibition leads to vasodilation
increases CTY, increases baroreceptor sensitivity, slows AV conduction to allow more filling time
give this in HF c HoTN and poor renal perfusion because is also alpha1 and alpha2-AR agonist as well as Beta-AR agonist
cause vasodilation via Beta-2 AR agonism, given IV in emergent HF sx
cause ionotropy (via increased cAMP in cardiac muscle) and vasodilation (by increases PKA)
recominant BNP, causes vasodilation and Na and water excretion
cause moderate Na channel block and increase AP duration by increasing phase 0 upstroke
mild Na channel block, shortens AP conduction
marked Na channel block, no effect on AP duration
blocks B-AR, decreases automaticity by decreasing the slope of phase 4 depolarization, blocks reentry by increasing refractory period and blocks catecholamine triggered arrhythmias
blocks DRK channels, prolongs reentry and causes AP duration to slow
Ca channel blockers, decrease slope of phase 4 depolarization and increase threshold potential by lowering HR
only terminates arrhythmias that go through AV node by decreasing K entry in AV node
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