EFFECT OF RENAL PERFUSION-PRESSURE ON RENAL INTERSTITIAL HYDROSTATIC-PRESSURE AND SODIUM-EXCRETION - ROLE OF VASOPRESSIN V-1 AND V-2 RECEPTORS

Renal interstitial hydrostatic pressure (RIHP) has recently been cited as an important mediator of pressure natriuresis. Our objective was to determine the roles of vasopressin V-1 and V-2 receptors in mediating the effects of renal perfusion pressure (RPP) on RIHP and sodium excretion (UNaV). The effects of RPP on renal hemodynamics, RIHP, and UNaV were assessed in control Wistar rats (n=10) and in rats pretreated with intravenous infusion of the specific nonpeptide vasopressin V-1 antagonist OPC-21268 (100 mu g.k(-1).min(-1); n=8) and the V-2 antagonist OPC-31260 (40 mu g.kg(-1).min(-1); n=10). Increasing RPP from 95 to 118 mm Hg in control rats increased RIHP (6.4+/-1.0 to 9.9+/-1.3 mm Hg), UNaV (0.29+/-0.03 to 0.52+/-0.05 mu Eq.min(-1).g(-1)), urine flow rate (UFR) (5.2+/-0.3 to 7.6+/-0.6 mu L.min(-1).g(-1)), and the fractional excretion of sodium (FE(Na)). In rats pretreated with V-1 antagonist, similar results were obtained for urine osmolality and the responses of RIHP, UNaV, UFR, and FE(Na) to RPP. V-2 antagonist reduced urine osmolality (392+/-47 compared with 979+/-88 mOsm.kg(-1) in control rats) and enhanced the responses of UNaV (0.43+/-0.08 to 1.32+/-0.32 mu Eq.min(-1)), UFR (17.8+/-3.2 to 29.2+/-3.8 mu L.min(-1).g(-1)), and FE(Na) to RPP, but the RIHP response resembled that observed in the control and V-1 antagonist groups. Renal blood flow and glomerular filtration rate did not differ among the three groups. Our findings indicate that neither V-1 nor V-2 receptor blockade influences the transmission of RPP into the renal interstitium, although V-2 receptor blockade enhances pressure natriuresis. The pressure natriuresis is mediated primarily by increased RIHP, and the enhanced natriuretic response to the V-2 antagonist is independent of RIHP.