Hemodynamic and antihypertensive treatment responses with calcium antagonists

Abstract

Calcium antagonists induce vasodilation and a consequent fall in blood pressure that initially is associated with baroreflex-mediated stimulation of the sympathetic nervous and renin-angiotensin system, resulting in increased heart rate and cardiac output. During chronic treatment, baroreflex-mediated stimulatory effects subside, probably because of a resetting of baroreflexes or inhibition of neuronal noradrenaline release. Ultimately, the antihypertensive response is codetermined by the responsiveness of these counterregulatory systems in the individual patient. In older patients who have blunted baroreflex and beta-adrenoceptor-mediated functions, a greater fall in blood pressure results as compared with younger patients in whom counterregulatory reflexes are more vivid. Therefore, older patients respond particularly well to calcium antagonists, whereas younger patients respond better to beta-blockers. In patients with essential hypertension, free cytosolic calcium concentration in platelets is elevated and calcium influx-dependent vasoconstriction is enhanced. Antihypertensive treatment with calcium antagonists and beta-blockers results in a normalization of both calcium influx-dependent vasoconstriction as well as free calcium concentration in platelets. Free cytosolic calcium concentration in platelets may reflect free calcium concentration in vascular smooth muscle cells, its reduction leading to vasodilation and antihypertensive response.