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1 zdepartment of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: majid{at}tulane.edu.
This study was performed to examine the role of superoxide (O2 -) formation in the regulation of renal hemodynamic and excretory function and to assess its contribution in the pathogenesis of angiotensin II (Ang II) dependent form of hypertension. Renal responses to acute intra-arterial infusion of the O2 - scavenger, tempol (50 µg/min/100g BW) with or without catalase (1500 U/min/100g; both native and PEG-catalase), that reduces H2O2, were evaluated in anesthetized male Sprague-Dawley rats treated chronically with Ang II (65 ng/min) for 2 weeks and compared to non-treated 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 non-treated normotensive rats did not cause significant changes in any of these renal parameters. Co-infusion of catalase with tempol did not alter the responses observed with tempol alone indicated 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, co-infusion of catalase reduced H2O2 excretion in both Ang II-treated (41±6%) and non-treated 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 contribute to the pathogenesis of Ang II - induced hypertension.
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