Vasodilating Drugs Flashcards
sodium nitroprusside
vasodilator –> spontaneous nonenzymatic NO release
nonspecific - dilates arteries AND veins (decrease afterload and preload)
HTN emergencies –> fast acting but toxicity limits use
**can cause cyanide accumulation –> NOT for patients with renal issues
what is the toxicity associated with sodium nitroprusside?
cyanide accumulation (–>cyanide–>thiocyanate –> kidneys)
can cause acid/base issues, arrhythmias, death
DO NOT USE WITH RENAL ISSUES
minoxidil
vasodilator, K+ channel opener
hyperpolarization causes arteriolar smooth m relaxation
doesnt affect veins
coadminister with B blocker to avoid reflex
BUT can evoke sympathetic reflex (increase HR, renin, contractility)
Rogaine
topical minoxidil
minoxidil, a K+ channel opener, increases hair growth
can have CV effects
what drug opens K+ channels?
minoxidil
hydralazine
oral directly vasodilates smooth m arterioles decreases TPR (afterload) and BP can cause sympathetic relfex(HR increase, renin retention) Use with pregnancy HTN
drug for HTN associated with pregnancy?
hydralazine
clonidine
CNS central acting vasodilator (sympathoLYTIC)
stimulates alpha2A receptor in brainstem to decrease sympathetic outflow!
BUT high doses reverse the effect –> activate alpha 2B on vascular smooth m and cause vasoconstriction
what happens with high doses of clonidine?
lose dilation effect
activates alpha 2B receptor in smooth m which causes vasoconstriction
alpha 2A vs alpha 2B receptors
2A is in CNS and causes vasodilation(decrease sympathetic)
2B is in vascular smooth m and vasoconstricts
guanadrel
false neurotransmitter that is inactive at postganglionic adrenergic receptors
taken up by NE transporter and replaces NE in vesicles
BUT there is potential for NE release so DONT USE WITH pheochromocytoma
risk of guanadrel?
since it is a false neurotransmitter there is a chance NE could be released
reserpine
binds to storage vesicles in CNS and PNS and inhibits transport and storage of NE/dopa
categories of ca channel blockers
dihydropyridine
non-dihydropyridine
vasodilating dihydropyridine? and nondihydropyridine?
di- nifedipine
non-verapamil
ca ch blockers (dihydro/nondihydro) effects
both act on smooth m (artery>venous) AND myocardium
inhibit L-type Ca channels
decreases contractility and Sa rate/av conductivity
dont affect skeletal muscle
verapamil
nondihydropyridine
L type ca ch blocker , affects vessels and heart
vasodilates vessels
decreases SA rate and AV conduction velocity
use: HTN and arrythmias
BUT can cause ecessive vasodilation, ,AV node block, and decreased CO
T/F: verapamil only affects smooth m?
FALSE
it affects vessels AND myocardium (SA rate and AV conduction v)
nifedipine
dihydropyridine
L type ca ch blocker, smooth m and myocardium
keeps intracellular Ca LOW
reflex causes increase in HR and contractility
use with heart failure