Abstract
In the rabbit cortical collecting duct (CCD) perfused in vitro, we recently found that luminal arginine vasopressin (AVP) hyperpolarizes the transepithelial voltage (Vt) and inhibits the hydrosmotic effect of basolateral AVP. The present study was undertaken to characterize the apical receptor of the CCD for AVP. In contrast to AVP, luminal application of 1-desamino-8-D-arginine vasopressin (DDAVP), a V2 agonist, did not significantly induce hyperpolarization. Luminal oxytocin (OXT) hyperpolarized Vt, interfering with the effect of superimposed luminal AVP, whereas [Thr4,Gly7]OXT, an OXT agonist, did not reproduce the effect of OXT. The effects of luminal AVP and OXT were abolished by [d(CH2)5,Tyr(Me)]-AVP, a V1 antagonist. Finally, luminal applications of AVP metabolite neuropeptides, pGlu-Asn-Cys(Cys)-Pro-Arg and pGlu-Asn-Cys(Cys)-Pro-Arg-Gly-NH2, were without effect on Vt. These data suggest that luminal AVP induces hyperpolarization through an apical V1 receptor but not through a V2 receptor or an OXT receptor.
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