Renal afferent and efferent arteriolar dilation by nilvadipine: Studies inthe isolated perfused hydronephrotic kidney

Although calcium antagonists are believed to exert preferential vasodilator action on the renal preglomerular afferent arteriole, we recently demonstr ated that efonidipine, a novel calcium antagonist, vasodilates both afferen t and efferent arterioles. Nilvadipine also is reported to increase renal b lood flow and reduce filtration fraction, suggesting indirectly afferent an d efferent arteriolar vasodilation. No direct investigation, however, has b een conducted examining the renal microvascular action of nilvadipine. We t herefore characterized the renal microvascular reactivity to nilvadipine, b y using the isolated perfused rat hydronephrotic kidney. The administration of angiotensin II (0.3 nM) caused marked vasoconstriction of afferent (fro m 13.5 +/- 0.6 to 9.2 +/- 0.6 mu m, p < 0.01, n = 6) and efferent arteriole s (from 11.5 +/- 1.0 to 7.4 +/- 0.7 mu m, < 0.01; n = 5). The subsequent ad dition of nilvadipine (10 nM, 100 nM, and 1 mu M) caused 37 +/- 5%, 91 +/- 4%, and 95 +/- 8% reversal of afferent arteriolar constriction, respectivel y. Similarly, efferent arterioles manifested 59 +/- 12% reversal by 1 mu M nilvadipine. Thus unlike nifedipine, which we previously reported to cause modest efferent arteriolar dilation (21 +/- 1% reversal at 1 mu M), nilvadi pine possesses the greater ability to dilate efferent arterioles (p < 0.01 vs. nifedipine), although both antagonists cause similar magnitudes of affe rent arteriolar vasodilation. Variable effects on the efferent arteriole su ggest the heterogeneity in the calcium antagonist with regard to the renal microvascular action of this agent.