The chief hemodynamic effect of selective calcium channel blockers is vasodilatation of the coronary and peripheral arteries, which reduces vascular resistance and improves blood flow.³ Nifedipine and the other dihydropyridines used to treat hypertension exert a potent vasodilatory effect on both the coronary and the peripheral vasculatures. Diltiazem produces coronary vasodilatation similar to that seen with nifedipine, but it is a less potent peripheral vasodilator than either nifedipine or verapamil. Verapamil's coronary vasodilatory activity is weaker than that of diltiazem or nifedipine, and its effect on the peripheral vasculature is intermediate between that of the other two drugs.¹¹.

All calcium channel blockers can produce negative inotropy.¹² Verapamil is the most powerful negative inotrope among the calcium channel blockers, followed by nifedipine.^13,14 Nifedipine's cardiodepressant effect is, however, largely overcome by reflex sympathetic stimulation, which boosts myocardial contractility and heart rate, at least initially. Unlike the dihydropyridines, verapamil and diltiazem are active in cardiac conductive tissue. By slowing conduction through the atrioventricular (AV) node and prolonging the AV node functional recovery period, they modulate heart rate (verapamil more so than diltiazem). Diltiazem also directly affects the sinus node, causing a small but consistent reduction in heart rate.

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