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Urotensin II is a nitric oxide-dependent vasodilator and natriuretic peptide in the rat kidney

¹Departments of Physiology and Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and ²Vascular Research, Johnson and Johnson Pharmaceutical Research and Development, Spring House, Pennsylvania 19477

Submitted 23 September 2002 ; accepted in final form 29 May 2003

Recent studies have indicated that urotensin II (UII), a cyclic peptide, is vasoactive and may be involved in cardiovascular dysfunctions. It remains unknown, however, whether UII plays a role in the control of renal vascular tone and tubular function. In the present study, a continuous infusion of synthetic human UII (hUII) into the renal artery (RA) in anesthetized rats was found to increase renal blood flow (RBF) and urinary water and sodium excretion (UV and U_NaV) in a dose-dependent manner. At a dose of 20 ng · kg^–1 · min^–1, it increased RBF by 20% and UV and U_NaV by 94 and 109%, respectively. Nitric oxide (NO) synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME) completely abolished hUII-induced increases in RBF and water/sodium excretion. In isolated, pressurized, and phenylephrine-precontracted small RA with internal diameter of 200 µm, hUII produced a concentration-dependent vasodilation with a maximal response of 55% at 1.5 µM. L-NAME significantly blocked this hUII-induced vasodilation by 60%. In denuded RA, hUII had neither vasodilator nor vasoconstrictor effect. With the use of 4,5-diaminofluorescein diacetate-based fluorescence imaging analysis of NO levels, hUII (1 µM) was shown to double the NO levels within the endothelium of freshly dissected small RA, and L-NAME blocked this UII-induced production of endothelial NO. These results indicate that UII produces vasodilator and natriuretic effects in the kidney and that UII-induced vasodilation is associated with increased endothelial NO in the RA.

natriuretic factor; renal circulation; sodium reabsorption; renal tubule; renal hemodynamics

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