anti-HTN drug MOA's Flashcards
Thiazide Diuretics
inhibit Na+ reabsorption in the distal tubule
Loop Diuretics
inhibits active transport of Na+, Cl. K+ in thick ascending loop of henle, causing excretion of ions
-in response, the collecting duct excretes more water
aldosterone receptor blockers
competes w/aldosterone, prevents sodium reabsorption and potassium excretion
Potassium sparing drugs
blocks Na reabsorption and K excretion, effect independent of aldosterone (aka no effect on aldosterone)
ACE-I
inhibit ACE to block production of AT II (blocks conversion of AT-1–> AT-2
inhibits breakdown of bradykinin (which is a vasodilator)
which is good obv a vasodilator lowers BP
bad because inflammatory mediator
dilates the efferent arteriole of kidney
ARB
inhibits angiotensin II at receptor site
does not inhibit breakdown of bradykinin (no cough)
Renin Inhibitor
Directly inhibits renin
renin is the major agent to tell angiotensinogen to start producing angiotensin I
Beta blockers
block beta 1 and or beta 2 receptors
decreasing the effects of EPI and NE which decreases the BP and HR
Non-Dihydropyridines CCB
inhibits calcium influex into CARDIAC smooth muscle: decreases rate/force contraction
Dihydropyradines CCB
inhibits calcium influx into VASCULAR smooth muscle: peripheral vasodilation
Alpha 1 blocker
competively inhibits alpha-1 receptors in periphery, causes vasodilation
Centrally acting alpha 2 agonists
stimulates alpha 2 receptors in the brain, reduces sympathetic outflow from the brain, produces a decreased BP and decreased peripheral vascular resistantce
Vasodilators
Direct vasodilator, especially in arteries and arterioles, leading to decreased systemic vascular resistance
causes peripheral vasodilation
