Modification by dihydropyridine-type calcium antagonists of the renal hemodynamic response to vasoconstrictors.

The effects of dihydropyridines on the renal response to vasoconstrictors was assessed using the isolated perfused rat kidney. During norepinephrine-induced vasoconstriction, dihydropyridines preferentially alter glomerular filtration rate and have less of an effect on perfusate flow. Calcium channel antagonists such as nitrendipine and nisoldipine augment glomerular filtration rate, whereas calcium channel agonists depress glomerular filtration rate. A preferential effect on glomerular filtration rate is also observed with the administration of nitrendipine to kidneys during vasoconstriction induced by angiotensin II. In contrast, nitrendipine does not exert a preferential augmentation of glomerular filtration during vasoconstriction mediated by KCl-induced depolarization. These observations are discussed in the context of the cellular mechanisms of dihydropyridines. It is proposed that differing postreceptor processes couple receptor occupation to smooth muscle contraction in afferent and efferent arterioles, and that a selective inhibition of receptor-mediated afferent vasoconstriction may underlie the renal hemodynamic response to dihydropyridines.