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Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisana
Submitted 7 March 2005 ; accepted in final form 8 August 2005
This study was performed to examine the role of superoxide formation in the regulation of renal hemodynamic and excretory function and to assess its contribution in the pathogenesis of ANG II-dependent hypertension. Renal responses to acute intra-arterial infusion of the O2– scavenger tempol (50 µg·min–1·100 g body wt–1) with or without catalase (1,500 U·min–1·100 g–1; both native and polyethylene glycol-catalase), which reduces H2O2, were evaluated in anesthetized male Sprague-Dawley rats treated chronically with ANG II (65 ng/min) for 2 wk and compared with nontreated control rats. In ANG II-treated hypertensive rats, tempol caused increases in medullary (13 ± 2%), cortical (5 ± 2%), and total renal blood flow (9 ± 2%) without altering systemic arterial pressure. There were also increases in glomerular filtration rate (9 ± 2%), urine flow (17 ± 4%), and sodium excretion (26 ± 5%). However, tempol infusion in nontreated normotensive rats did not cause significant changes in any of these renal parameters. Coinfusion of catalase with tempol did not alter the responses observed with tempol alone, indicating that the observed renal responses to tempol in ANG II-treated rats were attributed to its O2– scavenging effects without the involvement of H2O2. Tempol infusion also significantly decreased 8-isoprostane excretion in ANG II-treated rats (39 ± 6%) without changes in H2O2 excretion. However, coinfusion of catalase reduced H2O2 excretion in both ANG II-treated (41 ± 6%) and nontreated rats (28 ± 5%). These data demonstrate that enhanced generation of O2– modulates renal hemodynamic and tubular reabsoptive function, possibly leading to sodium retention and thus contributing to the pathogenesis of ANG II-induced hypertension.
superoxide; angiotensin II
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