L-arginine Stimulates NO-Dependent Vasodilation in Healthy Humans—Effect of Somatostatin Pretreatment

Abstract

Background

L-arginine is the precursor of endogenous nitric oxide (NO) and a potent stimulator of pituitary growth hormone and pancreatic insulin secretion. Both hormones have vasodilatory effects, which may be mediated via NO. We investigated whether growth hormone and/or insulin secretion contributes to L-arginine-induced vasodilation.

Methods

Ten healthy male subjects received an intravenous infusion of L-arginine, or L-arginine during somatostatin coinfusion lasting 30 minutes. Blood pressure, heart rates, and total peripheral resistance were assessed from 30 minutes prior to L-arginine infusion to 120 minutes after the start of the infusion. Plasma nitrite and cGMP concentrations were used as markers for endogenous NO formation.

Results

L-arginine significantly reduced total peripheral resistance, which remained decreased for 60 minutes after the end of the infusion. This resulted in a significantly lowered blood pressure. L-arginine elevated plasma nitrite and cGMP concentrations. Plasma growth hormone level showed a peak at 30 minutes after the infusion, while insulin and glucagon levels were maximal during the infusion, these endocrine effects were blocked during somatostatin coinfusion. The initial reduction in total peripheral resistance and blood pressure, and the elevation of nitrite and cGMP levels were still present during somatostatin cotreatment, but values returned to baseline more rapidly at the end of the L-arginine infusion.

Conclusion

We conclude that growth hormone contributes to the late phase of L-arginine-induced, NO-mediated vasodilation. By contrast, insulin did not mediate L-arginine induced vasodilation, as the early vasodilator effect, which occurred concomitantly with the peak insulin secretion, was still present after insulin secretion was blocked with somatostatin.