Calcium entry blockers and cardiovacular failure.
The beneficial influence of calcium entry blockers in the treatment of ischemia, both in the heart and in other tissues, can be explained by many effects including 1) relaxation of venous smooth muscle cells, in particular those of the splanchnic veins; 2) a negative inotropic effect on the myocardial cells; 3) negative chronotropic effects on the heart; 4) inhibition of vasospastic episodes in coronary and other large arteries; 5) depression of myogenic activity and responsiveness to vasoconstrictor stimuli in precapillary resistance vessels; 6) inhibition of platelet aggregation; 7) possibly, increases in the deformability of hypoxic red blood cells; 8) protection of endothelial integrity and function; and 9) protection of body cells, in particular myocardial cells, from prolonged exposure to anoxia and from massive entry of Ca2+ during reperfusion. In the case of angina pectoris, the effects on the myocardial cell itself, the decrease in preload and afterload, and the improvement of coronary perfusion combine to allow the patient to perform more work before unbalance is reached between the demands of the myocardial cells and their metabolic supply; the increased work performance favors collateral circulation and withdraws part of the reflex load on the heart that originates from the ischemic myocardium. The calcium entry blockers available vary in their potency to affect the different components of the cardiovascular system.
D000787:Angina Pectoris / Q000188:drug therapy*; D002121:Calcium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use*; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000188:drug therapy*; D006321:Heart / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism
D002121:Calcium Channel Blockers