Natriuretic peptide receptors mediate different responses in rat renal microvessels.

Atrial natriuretic peptide (ANP) has unique effects on the renal vasculature, in that it dilates preglomerular vessels and constricts efferent arterioles. In the present study we aimed to characterize the natriuretic peptide receptor (NPR) subtypes, which mediate the renovascular effects of ANP, using in vivo microscopy in the split hydronephrotic kidney model of rats. ANP (10(-9) and 3.10(-9)), which binds to NPR-A and NPR-C, dilated preglomerular vessels and constricted efferent arterioles similarly to that found in previous studies. C-type natriuretic peptide (10(-9) to 10(-7)), which binds to NPR-B and NPR-C, dilated pre- and postglomerular vessels and profoundly increased glomerular blood flow. A specific ligand of NPR-C, C-ANP (des-[Gln18,Ser19,Gly20,Leu21,Gly22]ANP 4-23-NH2, 10(-9) to 10(-7)) was devoid of vascular effects. The ANP antagonist A71915 (10(-9) to 10(-6)) induced moderate dilation in renal vessels possibly due to some agonistic activity on NPR-B, ANP-induced preglomerular vasodilation was attenuated by A71915 (10(-6)) to 36 +/- 6% of the initial response, whereas efferent vasoconstriction was completely abolished (-4 +/- 4% of initial response). Our results indicate that ANP dilates preglomerular vessels and constricts efferent arterioles through NPR-A, both responses being antagonized by A71915 with different potencies. Furthermore, our data show that in the rat renal microcirculation stimulation of NPR-B results in vasodilation only, whereas NPR-C does not mediate vascular responses.