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Am J Physiol Renal Physiol (June 3, 2003). doi:10.1152/ajprenal.00342.2002
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Submitted on September 23, 2002
Accepted on May 29, 2003

UROTENSIN II IS A NITRIC OXIDE-DEPENDENT VASODILATOR AND NATRIURETIC PEPTIDE IN THE RAT KIDNEY

Andrew Y. Zhang1, Ya-Fei Chen1, David X. Zhang1, Fu-Xian Yi1, Jenson Qi2, Patricia Andrade-Gordon2, Lawrence de Garavilla2, Pin-Lan Li1, and Ai-Ping Zou1*

1 Departments of Physiology and Pharmacology & Toxicology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Vascular Research, Johnson & Johnson Pharmaceutical Research & Development, L.L.C., Spring House, PA, USA

* To whom correspondence should be addressed. E-mail: azou{at}mcw.edu.

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 UNaV) in a dose-dependent manner. At a dose of 20 ng/kg/min it increased RBF by 20% and UV and UNaV by 94% and 109%, respectively. Nitric oxide synthase (NOS) inhibitor, 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. Using DAF-2DA-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 UII-induced vasodilation is associated with increased endothelial NO in the RA.




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