NATRIURETIC PEPTIDE RECEPTORS MEDIATE DIFFERENT RESPONSES IN RAT RENAL MICROVESSELS

Atrial natriuretic peptide (ANP) has unique effects on the renal vascu lature, in that it dilates preglomerular vessels and constricts effere nt arterioles. In the present study we aimed to characterize the natri uretic 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 arte rioles 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 p re- and postglomerular vessels and profoundly increased glomerular blo od Bow. A specific ligand of NPR-C, C-ANP (des-[Gln(18),Ser(19),Gly(20 ),Leu(21), Gly(22)]ANP(4-23)-NH2, 10(-9) to 10(-7)) was devoid of vasc ular effects. The ANP antagonist A71915 (10(-9) to 10(-6)) induced mod erate dilation in renal vessels possibly due to some agonistic activit y on NPR-B. ANP-induced preglomerular vasodilation was attenuated by A 71915 (10(-6)) to 36 +/- 6% of the initial response, whereas efferent vasoconstriction was completely abolished (-4 +/- 4% of initial respon se). Our results indicate that ANP dilates preglomerular vessels and c onstricts efferent arterioles through NPR-A, both responses being anta gonized by A71915 with different potencies. Furthermore, our data show that in the rat renal microcirculation stimulation of NPR-B results i n vasodilation only, whereas NPR-C does not mediate vascular responses .