Ginsenosides stimulate endogenous production of nitric oxide in rat kidney

Abstract

Ginsenosides (GS), saponins purified from Panax ginseng, increase renal blood flow in rats. Nitric oxide (NO) is thought to be the substance endogenously released by GS in preconstricted lungs and cultured endothelial cells. The present study aims to determine whether GS could stimulate endogenous release of NO in rat kidney and whether GS affected the activity of NO synthase in kidney tissues. The serum and urine levels of the stable NO metabolites, nitrite (NO 2) and nitrate (NO 3) and urinary cGMP levels were measured 8 hr after a single intraperitoneal injection of GS (200 mg/kg) into rats. The effects of the NO synthesis inhibitor, Nω-nitro-L-arginine methyl ester, and the NO precursor, L-arginine, on the GS-induced changes were also determined. The activity of NO synthase, as determined by conversion of [ 14C]-L-arginine to [ 14C]-L-citrulline, in whole kidney, glomeruli and cortical tubules was also investigated. A single injection of GS resulted in endogenous production of NO as reflected by increase in serum and urine levels of NO 2/NO 3 and urinary cGMP levels, which were inhibited by the addition of Nω-nitro-L-arginine methyl ester and restored by L-arginine. GS also stimulated the activity of NO synthase in whole kidney as well as glomeruli and cortical tubules, and this increase was significantly prevented by Nω-nitro-L-arginine methyl ester. It was concluded that stimulation in endogenous production of NO by GS may contribute to its antinephritic action and may play a protective role in the kidney.