The mechanism of action of calcium antagonists relative to their clinical applications.

As a class of therapeutic agents calcium antagonists have attracted increasing attention in recent years. Their major indications have been in the treatment of ischaemic myocardial syndromes, certain cardiac arrhythmias, hypertension, obstructive cardiomyopathies, and a number of lesser clinical disorders in which their role is less clearly defined. With the widening spectrum of therapeutic utility and an increasing plethora of newer agents under development, it is of importance to relate the overall pharmacodynamics of individual agents to their clinical effects. Calcium antagonists have a variable specificity for cardiac and peripheral activity. Based on such activity, it is useful to construct a classification of these compounds, new and old, into four categories. Type I agents, typified by verapamil and its congeners (tiapamil and gallopamil) and diltiazem, prolong AV nodal conduction and refractoriness with little effect on ventricular or atrial refractory period. These actions account for their direct antiarrhythmic properties. Type II agents include nifedipine and other dihydropyridines. In vivo, these agents are devoid of electrophysiologic effects in usual doses. They are potent peripheral vasodilators with some selectivity of action for different vascular beds; their overall haemodynamic effects are dominated by this peripheral vasodilatation and reflex augmentation of sympathetic reflexes. Type III agents include flunarizine and cinnarizine (piperazine derivatives), which, in vitro and in vivo, are potent dilators of peripheral vessels, with no corresponding calcium-blocking actions in the heart. Type IV agents are agents with a broader pharmacologic profile (perhexiline, lidoflazine and bepridil); they block calcium fluxes in the heart, in the peripheral vessels, or both. They may inhibit the fast channel in the heart and have other electrophysiologic actions. A clear understanding of the varied pharmacologic properties of the different classes of calcium antagonists is likely to provide a rational basis for the use of these agents in clinical therapeutics.

[1]  J. Alpert,et al.  Bepridil for chronic stable angina pectoris: results of a prospective multicenter, placebo-controlled, dose-ranging study in 77 patients. , 1984, The American journal of cardiology.

[2]  A. Fleckenstein History of Calcium Antagonists , 1983, Circulation research.

[3]  M. Piontek,et al.  Comparative electrophysiologic profiles of calcium antagonists with particular reference to bepridil. , 1985, The American journal of cardiology.

[4]  C. Haudenschild,et al.  Early Interactions Between Blood Cells and Severely Damaged Rabbit Aorta , 1971, European journal of clinical investigation.

[5]  W. Shapiro,et al.  The Effects of Lidoflazine on Exercise Performance and Thallium Stress Scintigraphy in Patients with Stable Angina Pectoris , 1982, Circulation.

[6]  R. N. Brogden,et al.  Flunarizine , 2012, Drugs.

[7]  L. Hillis,et al.  A controlled trial of verapamil for Prinzmetal's variant angina. , 1981, The New England journal of medicine.

[8]  K. Nademanee,et al.  Second-generation calcium antagonists: search for greater selectivity and versatility. , 1985, The American journal of cardiology.

[9]  C. R. Ingram,et al.  Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage. , 1983, The New England journal of medicine.

[10]  H. J. Gelmers Nimodipine, a New Calcium Antagonist, in the Prophylactic Treatment of Migraine , 1983, Headache.

[11]  R. O'rourke,et al.  Calcium entry blocking drugs: mechanisms of action, experimental studies and clinical uses. , 1985, Current problems in cardiology.

[12]  H. Hecht,et al.  Verapamil in chronic stable angina: amelioration of pacing-induced abnormalities of left ventricular ejection fraction, regional wall motion, lactate metabolism and hemodynamics. , 1981, The American journal of cardiology.

[13]  R. Bonow,et al.  Use of calcium-channel blocking drugs in hypertrophic cardiomyopathy. , 1985, The American journal of cardiology.

[14]  J. H. Comtor Harvey's 1651 perfusion of the pulmonary circulation of man. , 1982, Circulation.

[15]  H. Hecht,et al.  Comparative effects of oral verapamil and propranolol on exercise-induced myocardial ischemia and energetics in patients with coronary artery disease: single-blind placebo crossover evaluation using radionuclide ventriculography. , 1982, American heart journal.

[16]  E L Bolson,et al.  Dynamic mechanisms in human coronary stenosis. , 1984, Circulation.

[17]  F. Bühler,et al.  Calcium channel blockers: a pathophysiologically based antihyper onsive treatment concept for the future? , 1982, European journal of clinical investigation.

[18]  J. Cooper,et al.  Thromboxane Synthesis by Sources Other Than Platelets in Association with Complement‐Induced Pulmonary Leukostasis and Pulmonary Hypertension in Sheep , 1983, Circulation research.

[19]  B. Singh,et al.  Effects of bepridil on the electrophysiologic properties of isolated canine and rabbit myocardial fibers. , 1986, American heart journal.

[20]  K. Nademanee,et al.  Electrophysiologic and hemodynamic effects of slow-channel blocking drugs. , 1982, Progress in cardiovascular diseases.