The vasconstrictor vasopressin has been reported to induce paradoxical local vasodilation in the basilar vasculature through stimulation of the endothelium-derived relaxing factor nitric oxide (NO). We investigated the possibility that at subpressor doses, exogenous arginine vasopressin (AVP) might have a similar effect in the kidney. Ten Inactin-anesthetized rats were infused with sequential doses of AVP from 25 to 6,400 µU/min in 30-min increments. Subpressor infusion resulted in progressive renal vasodilation; renal blood flow (RBF) increased significantly going from 14 ± 6% above basal at 200 µU/min (p < 0.02) to 27 ± 5% (p < 0.01) at 1,600 µU/min accompanied by a 24 ± 5% decrease in renal vascular resistance (RVR). At 6,400 µU/min, blood pressure (BP) increased 29 ± 6 mm Hg and RVR increased. A second group of 8 rats were first given 10 mg/kg b.w. of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) before infusion of AVP. L-NAME increased BP 22 ± 3 mm Hg (p < 0.001), and decreased RBF 16 ± 3% (p < 0.005). After L-NAME, no dose of AVP had any further effect on either BP, RBF, or RVR. Continuous infusion of a single subpressor dose of 100 µU AVP resulted in a 26% increase in RBF (from 7.52 ± 0.68 to 9.49 ± 0.54 ml/min/g kidney weight, p < 0.001). AVP doubled urinary cyclic guanosine monophosphate excretion, a marker for renal NO synthesis, from 8.51 ± 1.01 to 17.48 ± 4.26 pM/min (p < 0.025). We conclude that AVP at subpressor doses induces renal vasodilation, which is eliminated by prior inhibition of NO synthesis.

Keywords:
Vasopressin, Nitric oxide, Endothelium, Renal vasodilation
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© 1995 S. Karger AG, Basel
1995
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