The present study was done to determine whether endogenous nitric oxide (NO) plays a role in the regulation of sodium transporters in the kidney. Male Sprague-Dawley rats were treated with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 4 weeks. Control rats were supplied with tap water without drugs. Expression of Na, K-ATPase, type 3 Na/H exchanger (NHE3), Na/K/2Cl cotransporter (BSC1), and thiazide-sensitive Na/Cl cotransporter (TSC) proteins was determined in the kidney by Western blot analysis. Catalytic activity of Na,K-ATPase was also determined. The treatment with L-NAME significantly and steadily increased the systemic blood pressure. Total and fractional excretion of urinary sodium decreased significantly, while creatinine clearance remained unaltered. Neither plasma renin activity nor aldosterone concentration was significantly altered. The alpha1 subunit expression and the catalytic activity of Na, K-ATPase were increased in the kidney. The expression of NHE3, BSC1 and TSC was also increased significantly. These results suggest that endogenously-derived NO exerts a tonic inhibitory effect on the expression of sodium transporters, including Na, K-ATPase, NHE3, BSC1, and TSC, in the kidney.
Animals ; Blotting, Western ; Carrier Proteins/*biosynthesis ; Enzyme Inhibitors/pharmacology ; Kidney/drug effects/metabolism ; Male ; NG-Nitroarginine Methyl Ester/*pharmacology ; Na(+)-K(+)-Exchanging ATPase/biosynthesis ; Nitric Oxide Synthase/*antagonists & inhibitors/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Drug/biosynthesis ; Sodium/*metabolism ; Sodium Chloride Symporters/biosynthesis ; Sodium-Hydrogen Antiporter/biosynthesis ; Sodium-Potassium-Chloride Symporters/biosynthesis