Effect of short-term high-protein compared with normal-protein diets on renal hemodynamics and associated variables in healthy young men.

BACKGROUND: High-protein diets are effective for weight reduction; however, little is known about the potential adverse renal effects of such diets. OBJECTIVE: The aim of our study was to compare the effect of a high-protein (HP) with a normal-protein (NP) diet on renal hemodynamics and selected clinical-chemical factors. DESIGN: We prospectively studied the effect of an HP diet (2.4 g x kg(-1) x d(-1)) with that of an NP diet (1.2 g x kg(-1) x d(-1)) on the glomerular filtration rate (assessed on the basis of sinistrin-an inulin analog-clearance) and renal plasma flow (para-aminohippuric acid clearance) by using the constant infusion technique. Filtration fraction and renal vascular resistance were calculated. Twenty-four healthy young men followed the 2 diet protocols for 7 d each in a crossover design. They were individually advised by a dietitian to achieve the planned protein intake by selecting normal foods under isocaloric conditions. Serum and urinary variables and renal hemodynamics were measured on day 7 of both diets. RESULTS: The glomerular filtration rate (NP: 125 +/- 5 mL/min; HP: 141 +/- 8 mL/min; P < 0.001) and filtration fraction (NP: 23 +/- 5%; HP: 28 +/- 5%; P < 0.05) increased significantly with the HP diet. Renal plasma flow was not significantly different between the HP (496 +/- 25 mL/min) and NP (507 +/- 18 mL/min) phases. Renal vascular resistance was not significantly different between the NP (94 +/- 6 mm Hg x mL(-1) x min(-1)) and HP (99 +/- 8 mm Hg x mL(-1) x min(-1)) phases. Blood urea nitrogen, serum uric acid, glucagon, natriuresis, urinary albumin, and urea excretion increased significantly with the HP diet. CONCLUSIONS: A short-term HP diet alters renal hemodynamics and renal excretion of uric acid, sodium, and albumin. More attention should be paid to the potential adverse renal effects of HP diets.

Rapid nongenomic effects of aldosterone on human forearm vasculature.

The impact of aldosterone in cardiovascular disease and hypertension has recently gained new interest. Aldosterone is now suggested to be a more common cause of hypertension than previously believed and has been linked to myocardial fibrosis, independent of its hypertensive effects. Finally, rapid nongenomic aldosterone effects have been proposed to be important in hypertension, in addition to its genomic effects. Forty-eight healthy male volunteers were examined in a randomized, placebo-controlled, double-blind crossover trial to elucidate the rapid nongenomic, vascular effects of aldosterone in humans. Forearm blood flow was measured by venous occlusion plethysmography. First, aldosterone (500 ng/min) and placebo were infused into the brachial artery for 8 minutes. The volunteers then received ascending doses of acetylcholine, NG-monomethyl-L-arginine (L-NMMA), sodium nitroprusside, or phenylephrine. Aldosterone increased forearm blood flow (P<0.001, ANOVA). The maximum effect was an increase in forearm blood flow with aldosterone of 7.9+/-2.6% compared with 0.1+/-1.9% with placebo treatment after 8 minutes. With aldosterone, L-NMMA induced a greater vasoconstriction (P<0.05, ANOVA), sodium nitroprusside induced an attenuated vasoconstriction (P<0.01, ANOVA), and phenylephrine induced an exaggerated vasoconstriction (P<0.01, ANOVA) within minutes as compared with placebo. These data suggest that aldosterone acts through rapid nongenomic effects at the endothelium by increasing NO release and at the vascular smooth muscle cells by promoting vasoconstriction. This is consistent with in vitro data showing an increase in intracellular calcium in both cell types. Disturbances of these aldosterone effects on both levels might be important in promoting hypertension.