INFLUENCE OF DIETARY-SODIUM INTAKE ON RENAL MEDULLARY NITRIC-OXIDE SYNTHASE

We previously reported that chronic systemic treatment of rats with a nitric oxide synthase inhibitor leads to a selective decrease in renal medullary blood flow, retention of sodium, and the development of hyp ertension. In the present studies, we used protein blotting techniques to determine the whole tissue distribution and relative quantitation of the different nitric oxide synthase isoforms in the renal cortex an d medulla of Sprague-Dawley rats maintained on a low (0.4% NaCl) or hi gh (4.0% NaCl) dietary salt intake. Neural, endothelial, and inducible nitric oxide synthase were readily detectable in homogenized renal in ner and outer medullas. Only endothelial nitric oxide synthase was det ectable in the renal cortex. Densitometric comparison of Western blots from equal amounts of total inner medullary tissue protein indicated that endothelial, inducible, and neural nitric oxide synthase were inc reased by 145%, 49%, and 119%, respectively, in rats maintained on a h igh NaCl diet compared with rats on a low NaCl diet. No significant di fferences in nitric oxide synthase levels were detected in the outer m edulla, renal cortex, or aorta of rats maintained on low and high NaCl diets. In separate studies, continuous intravenous infusion of N-G-ni tro-L-arginine methyl ester (8.6 mg/kg per day) for 11 days in chronic ally instrumented rats increased mean arterial pressure 32+/-3 mm Hg i n rats on a high NaCl diet (n=5) but only increased pressure 17+/-3 mm Hg in rats on a low NaCl diet (n=6). These data indicate that increas ed levels of renal medullary nitric oxide synthase may be important in the chronic adaptation to increased sodium intake.