Vasodilators etc Flashcards
Long-term outpatient therapy of severe or resistant hypertension
Hydralazine
Hypertensive emergencies
nitroprusside
Hypertensive emergencies; angina
Nitrates
- Long-term outpatient therapy of hypertension
- hypertensive emergencies
- angina
Verapamil
diltiazem
nifedipine
amlodopine
Reduction of calcium influx
Hyperpolarization of smooth muscle membrane through opening of potassium channels
Minoxidil
Diazoxide
Long-term outpatient therapy of severe or resistant hypertension
Minoxidil
-Hyperpolarization of smooth muscle membrane through opening of potassium channels
Hypertensive emergencies (and not a NO releaser)
Diazoxide
-Hyperpolarization of smooth muscle membrane through opening of potassium channels
Hypertensive emergencies, and not a NO releaser, potassium channel opener, or a calcium influx inhibitor
Fenoldopam: Activation of dopamine receptors
excessive hypotension, dizziness, headache, peripheral edema, flushing, tachycardia, rash, and gingival hyperplasia have been reported
Dihydropyridines
Dizziness, headache, peripheral edema, AV block, bradycardia, heart failure, lupus-like rash, pulmonary edema, coughing, and wheezing are possible
diltiazem
Dizziness, headache, peripheral edema, constipation, AV block, bradycardia, heart failure, pulmonary edema, coughing, and wheezing are possible
verapamil, non-DHP
slow heart rate, can slow atrioventricular conduction, can cause heart block, and are contraindicated in patients also taking a beta-blocker
Non-DHPs (verapamil > diltiazem)
does not decrease AV conduction and therefore can be used more safely than non-DHPs in the presence of AV conduction abnormalities
Nifedipine
may increase digoxin blood levels through a pharmacokinetic interaction
verapamil
Additive with other vasodilators
DHPs
Additive with other cardiac depressants and hypotensive drugs
non-DHPs
Long-term outpatient therapy of hypertension; hypertensive emergencies; angina
CALCIUM CHANNEL BLOCKERS
prototype DHPs, MOA
Amlodipine and nefidipine
MOA: Blocks L-type calcium channels in vasculature > cardiac channels
Prototype non-DHP drugs, MOA
Non-Dihydropyridines
(1) Prototypes: Verapamil, Diltiazem
(2) MOA: Nonselective block of vascular and cardiac L-type calcium channels
- cause vasodilation–> decreases peripheral resistance
- arterioles are more sensitive than veins
- orthostatic hypotension is not usually a problem
- relaxation of arteriolar smooth muscle leads to decreased afterload and decreased O2 demand by the heart
Ca channel blockers (CCBs)
CCBs: block channels in smooth muscle at much lower concentrations
non-DHPs: this is significant because while they have more cardiac effects, their cardiac effects are negligible at effective therapeutic concentrations
(t1/2) of 35-50 hours
amlodipine: the other CCBs typically 2-12 hrs