MOA & effects Flashcards
inhibit neurotrasmitter release from peripheral α2 receptors & depletion of neurotransmitters from vesicles through competitive uptake. Mainly peripherally acting.
Postganglionic adrenergic, α2 neuron blockers
block central α2 recepotors = decrease in sympathetic outflow to cardiovascular system
Centrally acting α2 agonist
non selecive blocker of peripheral α1 postsynaptic receptors
Peripherally acting α1 blockers
Inhibition of Na/Cl- symporter in distal convoluted tubules
Thiazide diuretics
This class blocks sodium reabsroption which leads to a decrease in Na, water, K, H, but an increase in Ca
Thiazide diuretics
Inhibition of Na-K-2Cl symproter in the ascending loop of Henle & distal tubule
Loop diuretics
This class blocks reabsroption of Na & Cl which leads to a decrease in Na, water, K,Cl, Mg & Ca
loop diuretics
iDisruption of the Na/K ATPase at the distal tubule & collecting ducts cause an increase in Mg, K and a decrease in Ca & Na
Potassium sparing diuretics
This agent competitive inhibitor of aldosterone at the distal tubules causing an increase in K & H but a decrease in Na, Cl, water
Spironolactone
By selectively blocking mineralocorticoid receptors in the kidney, heart, blood vessels & brain, this agent reduces BP
eplerenone
Competitively blocks norepi & epi from binding to beta-receptors on nerves
beta blockers
the overall effects of beta blockers includes:
heart rate reduction (neg chronotrop): bradycardia
vasodilation = lower BP
bronco-constriction
Block voltage gated calcium channels of cardiac & smooth muscle, lowering the intracellular calcium
Calcium channel blockers
The net effect of calcium channel blockers is
reduction in muscle contraction (neg inotrop)
vasodilaton = lower BP
DHP = positive chronotrop = tacychardia
NDHP = negative chronotrop = bradycardia
alpha-1 blockers cause an overall effect of:
Vasodilation of veins & arterioles –>
decreased total peripheral resistance
lower BP