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Class/MOA

Drug Classes and MOA for matching

QuestionAnswer
Direct Vasodilators Cause direct relaxation of peripheral arterial smooth muscle.
Calcium Antagonists Inhibit the influx of calcium through slow channels in vascular smooth muscle in both coronary and peripheral arteries. Cause SA and AV nodal depression.
CCB NonDHP Same as CCB, also decrease myocardial contractility.
Beta Blockers Block secretion of renin, decrease cardiac contractility/output, heart rate, and central sympathetic output.
Thiazide Diuretics Direct Arteriole dilation, reduction of total fluid volume by blocking Sodium reabsorption in the distal tubules (causing increased excretion of Na, H2o, K, H).
Loop Diuretics Reduction of total fluid volume by inhibition of sodium and chloride reabsorption in the ascending loop of Henle (causing increased excretion of H20, Na, Ca, Mg, Cl).
Potassium-Sparing Diuretics Interfere with potassium and sodium exchange in the distal tubule (causing increased Mg excretion and decreasing Ca excretion).
Adrenergic Inhibitors (Postganglionic) Cause presynaptic inhibition of Neurotransmitter from peripheral neurons by antagonizing a-2 receptor and depletion of neurotransmitter through competitive uptake into neurosecretory vesicles.
Adrenergic inhibitors (Centrally active a-2 agonists) Decrease sympathetic outflow to the cardiovascular system by agonistic activity on central a-2 receptors.
Adrenergic Inhibitors (Peripherally acting a-1 blockers) Blocks a-1 receptors causing vasodilation of both arteries and veins (indirect vasodilation)
ACE-I Inhibit conversion of AT-I to AT-II, indirectly inhibit fluid volume by inhibiting AT-II-stimulated release of aldosterone.
ARB Inhibit binding of AT-II to receptor preventing vasoconstriction and release of aldosterone.
Direct Renin Inhibitor Competitively inhibits Renin decreasing the conversion of AT to AT-1.
Created by: savejoseph
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