Renal hemodynamic effects of dietary protein in the rat: role of nitric oxide

The biologic mediator(s) of the renal hemodynamic effects of a high dietary protein intake (hyperfiltration and renal vasodilation) are unknown. The endogenous nitrovasodilator nitric oxide (NO) derives from the amino acid L-arginine, and NO has been demonstrated to mediate the hyperfiltration and vasodilation observed during amino acid infusion in rats. We therefore hypothesized that NO may also mediate the long-term renal hemodynamic effects of variations in dietary protein intake. We studied rats maintained with low protein (6%) and high-protein (50%) diets for 2 weeks. An additional group of rats receiving a high-protein diet was also treated with the NO synthase inhibitor, L-nitro-arginine-methyl ester (NAME, 100 mg per liter of drinking water). After 2 weeks a high-protein diet was associated with a significant increase in glomerular filtration rate (GFR) (50% protein group vs 6% protein group, 1.01 +/- 0.03 vs 0.61 +/- 0.03 ml/min; p < 0.05) and renal vasodilation (renal vascular resistance: 50% protein group vs 6% protein group, 11.70 +/- 0.88 vs 17.65 +/- 1.55 mm Hg/min/ml; p < 0.05) compared with a low-protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)