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318 SECTION III CARDIOvASCuLAR ``CARdIOvASCulAR—PHARMACOlOGY CARDIOvASCuLAR ``CARdIOvASCulAR—PHARMACOlOGY
Calcium channel Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act on vascular
blockers smooth muscle); diltiazem, verapamil (non-dihydropyridines, act on heart).
MECHANISM Block voltage-dependent L-type calcium channels of cardiac and smooth muscle muscle
contractility.
Vascular smooth muscle—amlodipine = nifedipine > diltiazem > verapamil.
Heart—verapamil > diltiazem > amlodipine = nifedipine (verapamil = ventricle).
ClINICAl uSE Dihydropyridines (except nimodipine): hypertension, angina (including vasospastic type), Raynaud
phenomenon.
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm).
Nicardipine, clevidipine: hypertensive urgency or emergency.
Non-dihydropyridines: hypertension, angina, atrial fibrillation/flutter.
AdvERSE EFFECTS Gingival hyperplasia.
Dihydropyridine: peripheral edema, flushing, dizziness.
Non-dihydropyridine: cardiac depression, AV block, hyperprolactinemia (verapamil), constipation.
Hydralazine
MECHANISM cGMP smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction.
ClINICAl uSE Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy.
Frequently coadministered with a β-blocker to prevent reflex tachycardia.
AdvERSE EFFECTS Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina,
drug-induced lupus.
Hypertensive Treat with labetalol, clevidipine, fenoldopam, nicardipine, nitroprusside.
emergency
Nitroprusside Short acting vasodilator (arteries = veins); cGMP via direct release of NO. Can cause cyanide
toxicity (releases cyanide).
Fenoldopam Dopamine D 1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation. BP,
natriuresis. Also used postoperatively as an antihypertensive. Can cause hypotension and
tachycardia.
Nitrates Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate.
MECHANISM Vasodilate by NO in vascular smooth muscle in cGMP and smooth muscle relaxation.
Dilate veins >> arteries. preload.
ClINICAl uSE Angina, acute coronary syndrome, pulmonary edema.
AdvERSE EFFECTS Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache, “Monday disease” in
industrial exposure: development of tolerance for the vasodilating action during the work week
and loss of tolerance over the weekend tachycardia, dizziness, headache upon reexposure.
Contraindicated in right ventricular infarction, hypertrophic cardiomyopathy, and with
concurrent PDE-5 inhibitor use.
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