Effects of calcium channel blockers on systemic hemodynamics in hypertension

Increased total peripheral resistance is the hemodynamic abnormality that characterizes established essential hypertension. Therefore, an antihypertensive agent should reduce arterial pressure by decreasing total peripheral resistance while maintaining systemic flow as well as flow to the target organs of hypertensive disease: the brain, heart, and kidney. Drugs that reduce total peripheral resistance have been used for many years. However, their stimulation of renal and humoral responses counteracts the antihypertensive effect and thereby limits their efficacy. Thus, when total peripheral resistance is reduced, the sympathetic nervous system and the renin-angiotensin system are activated. Increases in myocardial contractility, sympathetic tone, and angiotensin-mediated vasoconstriction; sodium and fluid retention; and tachycardia may result, thereby blunting the drug-induced decrease in arterial pressure and producing so-called "pseudoresistance" to the antihypertensive regimen. Most calcium channel blockers appear to differ from other vasodilators because neither the renin-angiotensin system nor the sympathetic nervous system is stimulated during long-term treatment. Moreover, in patients with left ventricular hypertrophy, certain calcium channel blockers allow left ventricular hypertrophy to regress.