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Articles in PresS, published online ahead of print March 12, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00270.2001
Submitted on August 27, 2001
Accepted on March 2, 2002
1 Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado, USA
* To whom correspondence should be addressed. E-mail: robert.schrier{at}uchsc.edu.
ARF contributes substantially to the high morbidity and mortality observed during endotoxemia. We hypothesized that selective blockade of the renal nerves would be protective against ARF during the early (16hours) stage of endotoxemia (i.p. injection of lipopolysaccride (LPS) 5mg/kg in mice). At 16 h after LPS, there was no change in mean arterial pressure (MAP) but plasma epinephrine (4604±719 vs 490±152pg/ml, P<0.001), norepinephrine (2176±306 vs 1224±218pg/ml, p<0.05) and plasma renin activity (40±5 vs 27±2 ng/ml/hr, p<0.05) were higher in the LPS treated versus control mice. The high PRA level decreased to the control level with renal denervation in endotoxemic mice. After intravenous injection of phentolamine (200µg/kg), the decrement in MAP was significantly greater in LPS treated versus control mice (19.4±3.5 vs 8.1±1.5mmHg, P<0.01). 16h after LPS administration, there were significant decreases in GFR (52±18 vs 212±23µl/min, p<0.01) and RBF (0.58±0.08 vs 0.85±0.06ml/min, p<0.01) in sham operated mice. The decrement in GFR during endotoxemia was significantly attenuated in mice with denervated kidneys (32% vs 79%). Moreover, there was no change in RBF during endotoxemia in mice with renal denervation. The present results therefore demonstrate a protective role of renal denervation during normotensive endotoxemia-related ARF in mice, an effect which may be, at least in part, due to a diminished activation of the renin-angiotensin system.
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