Abstract

Recently, attention has focused on the effects of calcium antagonists on renal function. When administered in vitro to the isolated perfused kidney, calcium antagonists exhibit consistent actions, permitting characterization of their renal effects. Calcium antagonists do not affect the vasodilated isolated perfused kidney, but they do dramatically alter the response of the kidney to vasoconstrictor agents. In the presence of norepinephrine, calcium antagonists markedly augment the glomerular filtration rate, but produce only a modest improvement in renal perfusion. By use of the postischemic, hydronephrotic rat kidney model, which permits direct visualization of afferent and efferent arterioles, it can be demonstrated that the above-mentioned preferential augmentation of glomerular filtration rate may be attributable to a selective vasodilation of preglomerular vessels. Although the clinical implications of such observations are not yet clear, preliminary studies in experimental animal models indicate that calcium antagonists might exert salutary effects on renal function in clinical settings characterized by impaired renal hemodynamics. There is a need to carry out prospective studies to determine the benefits of calcium antagonists in ameliorating the development of renal dysfunction in patients at risk of acute renal insufficiency.

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