Calcium antagonists differ from one another in terms of their potency, tissue selectivity, and duration of action. The calcium antagonists available for clinical use are mainly L-type channel blockers. The T channel appears at more negative potentials and seems to play a role in the initial depolarization of the sinus node and atrioventricular (AV) node tissue. Mibefradil, a T channel blocker, caused bradycardia and a host of adverse effects that caused the drug’s premature withdrawal from the market.channels. These agents cause dilation of coronary arteries and marked peripheral arteriolar dilatation resulting in a profound fall in blood pressure. There is little or no action on the sinoatrial (SA) node and conducting tissue.
Verapamil and diltiazem are phenylalkylamines and benzothiazepines. They cause distortion of calcium chan¬nels and coronary artery dilation, but there are additional effects on the SA and AV nodes. These agents also have a negative inotropic effect and decrease myocardial contrac¬tility. Thus, the dihydropyridines, phenylalkylamines, and benzodiazepines have vastly different actions. For example, only amlodipine and felodipine, of the dihydropyridine family, have proved relatively safe in patients with left ventricular dysfunction and heart failure. Other agents may precipitate heart failure. The hemodynamic and electrophysiologic effects of calcium antagonists are given in Table 1.

Страницы: 1 | 2