Pathophysiology of hypertension: effects of calcium antagonists on heart and kidney.

Hypertension is a multifactorial disease that is manifested hemodynamically by an increased total peripheral resistance that is more or less uniformly distributed throughout the organ circulations, especially in its target organs, the brain, heart, and kidney. The vasoconstriction involves venules as well as arterioles. The increased afterload that is imposed upon the left ventricle results in the development of concentric hypertrophy. This may be complicated by a preload component early in hypertension or in patients who are volume-dependent (e.g., obesity, blacks). Eventually, if not treated, dysrhythmias, sudden death, or cardiac failure may supervene. The kidney becomes affected by progressive failure in function related to hemodynamic impairment secondary to afferent, as well as efferent, arteriolar constriction, which increases glomerular hydrostatic pressure. If at all possible, antihypertensive therapy should not be associated with intravascular volume expansion or reflex cardiac stimulation. Calcium antagonists reduce arterial pressure through a fall in vascular resistance without expanding volume or inordinately stimulating the heart. Left ventricular afterload is diminished with associated decrease of left ventricular mass. Moreover, renal blood flow increases while filtration fraction and glomerular hydrostatic pressure diminishes. Thus, these agents approach the ideal in reversing the pathophysiological complications of the disease.