Effects of nitric oxide synthesis inhibition on the Na,K-ATPase activity in the kidney.

The present study was aimed at investigating the role of endogenous nitric oxide (NO) in regulating Na,K-ATPase activity in the kidney. The expression of alpha-1 and beta-1 subunits; and the enzymatic activity of Na,K-ATPase were determined in the kidney of rats treated with an NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). Following the treatment with L-NAME in the drinking water for 4 weeks, Na,K-ATPase activity was increased while tissue nitrite/nitrate levels were decreased in the kidney. Supplementation with L-arginine prevented the L-NAME-induced changes. The expression of either alpha-1 or beta-1 subunit protein of Na,K-ATPase, assessed by Western blot analysis, was not affected by L-NAME-treatment. An acute in vitro treatment of the kidney with L-NAME also caused an increase of Na,K-ATPase activity; which was again prevented by cotreatment with L-arginine. On the contrary, treatment with sodium nitroprusside significantly decreased Na,K-ATPase activity. These results suggest that the endogenous NO plays a direct inhibitory role on Na,K-ATPase activity in the kidney.