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1 Nephrology, INC Ignacio Chavez, Mexico City, Mexico
2 Nephrology, INC Ignacio Chávez, Mexico City, D.F., Mexico
3 Pathology, INC Ignacio Chavez, Mexico City, D.F., Mexico
4 Mexico City, DF, Mexico; Nephrology, INC Ignacio Chavez, Mexico City, Mexico
5 Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, Florida, United States
* To whom correspondence should be addressed. E-mail: lgsanchezlozada{at}hotmail.com.
Experimental hyperuricemia (HU) results in preglomerular arteriolopathy, cortical vasoconstriction and glomerular hypertension. Recently uric acid has been shown to induce endothelial dysfunction. We therefore studied the effect of acute and chronic administration of L-arginine (substrate for endothelial nitric oxide synthase) on the renal hemodynamic and vascular structural alterations induced by HU. To induce HU, oxonic acid (OA, 750 mg/kg/day), was administered in male Sprague-Dawley rats.. To study the acute effect of arginine, 9 rats received L-arginine (L-Arg, 15 mg/kg/min) during micropuncture. To elucidate the chronic effect of L-Arg, OA+ 1% L-Arg (n=8) and OA+ 2.5% L-Arg (n=6) (drinking water) were evaluated throughout the 5 week period. Eight normal control (N),and 8 OA, rats were also studied. Kidneys were fixed by perfusion and afferent arteriole morphology was evaluated. HU rats developed the renal functional and structural alterations described and had suppressed urinary excretion of NO-2/NO-3. Acute stimulation of NO synthesis markedly increased urinary NO-2/NO-3, lowered systemic blood pressure and relieved cortical vasoconstriction despite a significant increment of glomerular hypertension and afferent arteriole damage. Increasing doses of chronic L-Arg were associated with increasing excretion of urinary NO-2/NO-3, reduction of systemic hypertension and prevention of cortical vasoconstriction (2.5% L-Arg). In addition, both doses prevented glomerular hypertension and preglomerular arteriolopathy. Thus an acute relief of renal vasoconstriction in the setting of afferent arteriole damage cannot reverse glomerular hypertension, likely due to impairment in preglomerular autoregulation. On the other hand chronic L-Arg preserved arteriolar structures probably mediated by the antiproliferative effect of NO on VSMC.
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