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Am J Physiol Renal Physiol 282: F991-F997, 2002. First published January 2, 2002; doi:10.1152/ajprenal.00283.2001
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Vol. 282, Issue 6, F991-F997, June 2002

Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure-independent mechanism

Marilda Mazzali, John Kanellis, Lin Han, Lili Feng, Yi-Yang Xia, Qiang Chen, Duk-Hee Kang, Katherine L. Gordon, Susumu Watanabe, Takahiko Nakagawa, Hui Y. Lan, and Richard J. Johnson

Division of Nephrology, Baylor College of Medicine, Houston, Texas 77030

Hyperuricemia is associated with hypertension and vascular disease, but whether this represents a causal relationship or an epiphenomenon remains unknown. We recently reported a model of mild hyperuricemia in rats that results in increased blood pressure and mild renal fibrosis. In this study, we examined the effect of hyperuricemia on the renal vasculature. Rats fed 2% oxonic acid and a low-salt diet for 7 wk developed mild hyperuricemia (1.8 vs. 1.4 mg/dl, P < 0.05), hypertension [147 vs. 127 mmHg systolic blood pressure (SBP), P < 0.05], and afferent arteriolar thickening, with a 35% increase in medial area (P < 0.05). Allopurinol or benziodarone prevented the hyperuricemia, hypertension, and arteriolopathy. Hydrochlorothiazide treatment did not prevent the hyperuricemia or arteriolopathy despite controlling blood pressure. In contrast, the arteriolopathy and hypertension were prevented by both enalapril and losartan. Uric acid also directly stimulated vascular smooth muscle cell proliferation in vitro, and this was partially inhibited by losartan. Thus hyperuricemia induces a renal arteriolopathy in rats that is blood pressure independent and involves the renin-angiotensin system.

uric acid; hypertension; angiotensin II


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