Calcium-entry blockers and vascular smooth muscle.
Calcium-entry blockers depress the myogenic activity and the responsiveness to vasoconstrictor stimuli of the smooth muscle cells of the precapillary vessels. Thus, they can reduce the afterload of the heart and have antihypertensive properties. Their inhibitory effect on the contractile responses of the vascular smooth muscle cells of large arteries also results in the reduction or the abolition of vasospastic episodes. By inhibiting the constrictor responses of the splanchnic capacitance vessels to the sympathetic nervous outflow, they reduce the preload of the heart. However, different calcium-entry blockers differ in their ability to affect different cardiovascular variables and in the onset and duration of their effect; they also have different degrees of tissue selectivity. This variability must reflect differences in pharmacodynamic and pharmacokinetic properties.
D000787:Angina Pectoris / Q000503:physiopathology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D002395:Catecholamines / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy; D006801:Humans; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D009638:Norepinephrine / Q000502:physiology; D011188:Potassium / Q000502:physiology
D002121:Calcium Channel Blockers; D002395:Catecholamines; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine