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(Hypertension. 1995;25:866-871.)
© 1995 American Heart Association, Inc.

Articles

Effect of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Sodium Excretion

Role of Vasopressin V₁ and V₂ Receptors

Tetsuya Nakamura; Tetsuo Sakamaki; Toshiaki Kurashina; Kunio Sato; Zenpei Ono; Kazuhiko Murata

From the Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.

Correspondence to Tetsuya Nakamura, MD, The Second Department of Internal Medicine, Gunma University School of Medicine, Maebashi, 371, Japan.

Abstract 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 V₁ and V₂ receptors in mediating the effects of renal perfusion pressure (RPP) on RIHP and sodium excretion (U_NaV). The effects of RPP on renal hemodynamics, RIHP, and U_NaV were assessed in control Wistar rats (n=10) and in rats pretreated with intravenous infusion of the specific nonpeptide vasopressin V₁ antagonist OPC-21268 (100 µg · kg^-1 · min^-1; n=8) and the V₂ antagonist OPC-31260 (40 µg · 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), U_NaV (0.29±0.03 to 0.52±0.05 µEq · min^-1 · g^-1), urine flow rate (UFR) (5.2±0.3 to 7.6±0.6 µL · min^-1 · g^-1), and the fractional excretion of sodium (FE_Na). In rats pretreated with V₁ antagonist, similar results were obtained for urine osmolality and the responses of RIHP, U_NaV, UFR, and FE_Na to RPP. V₂ antagonist reduced urine osmolality (392±47 compared with 979±88 mOsm · kg^-1 in control rats) and enhanced the responses of U_NaV (0.43±0.08 to 1.32±0.32 µEq · min^-1), UFR (17.8±3.2 to 29.2±3.8 µL · min^-1 · g^-1), and FE_Na to RPP, but the RIHP response resembled that observed in the control and V₁ antagonist groups. Renal blood flow and glomerular filtration rate did not differ among the three groups.

Our findings indicate that neither V₁ nor V₂ receptor blockade influences the transmission of RPP into the renal interstitium, although V₂ receptor blockade enhances pressure natriuresis. The pressure natriuresis is mediated primarily by increased RIHP, and the enhanced natriuretic response to the V₂ antagonist is independent of RIHP.

Key Words: vasopressin • renal blood flow • pressure natriuresis • glomerular filtration rate