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1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
* To whom correspondence should be addressed. E-mail: dmattson{at}mcw.edu.
Experiments in wild-type (WT; C57BL/6J) mice, endothelial nitric oxide synthase null mutant (eNOS-/-) mice, and neuronal NOS null mutant (nNOS-/-) mice were performed to determine which NOS isoform regulates renal cortical and medullary blood flow under basal conditions and during the infusion of angiotensin II (Ang II). Inhibition of NOS with N
-nitro-L-arginine methyl ester (L-NAME; 50 mg/kg iv) in Inactin-anesthetized WT and nNOS(-/-) mice increased arterial blood pressure by 28-31 mmHg and significantly decreased blood flow in the renal cortex (18-24%) and the renal medulla (13-18%). In contrast, blood pressure and renal cortical and medullary blood flow were unaltered following L-NAME administration to eNOS(-/-) mice, indicating that NO derived from eNOS regulates baseline vascular resistance in mice. In subsequent experiments, intravenous AngII (20 ng/kg/min) significantly decreased renal cortical blood flow (by 15-25%) in WT, eNOS(-/-), nNOS(-/-), and WT mice treated with L-NAME. The infusion of AngII, however, led to a significant increase in medullary blood flow (12-15%) in WT and eNOS(-/-) mice. The increase in medullary blood flow following AngII was not observed in nNOS(-/-) mice, in WT or eNOS(-/-) mice pretreated with L-NAME, or in WT mice administered the nNOS inhibitor 5-(1-imino-3-butenyl)-L-ornithine (1 mg/kg/h). These data demonstrate that NO from eNOS regulates baseline blood flow in the mouse renal cortex and medulla while NO produced by nNOS mediates an increase in medullary blood flow in response to AngII.
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