THE VASCULAR EFFECTS OF L-ARGININE IN HUMANS - THE ROLE OF ENDOGENOUSINSULIN

This study aimed at evaluating whether increased availability of the n atural precursor of nitric oxide, L-arginine, could influence systemic hemodynamic and theologic parameters in humans and whether the effect s of L-arginine are mediated by endogenous insulin. 10 healthy young s ubjects participated in the following studies: study I, infusion of L- arginine (1 g/min for 30 min); study II, infusion of L-arginine plus o ctreotide(25 mu g as i.v. bolus + 0.5 mu g/min) to block endogenous in sulin and glucagon secretion, plus replacement of basal insulin and gl ucagon; study III, infusion of L-arginine plus octreotide plus basal g lucagon plus an insulin infusion designed to mimic the insulin respons e of study I. L-Arginine infusion significantly reduced systolic (11+/ -3, mean+/-SE) and diastolic (8+/-2 mmHg, P < 0.001) blood pressure, p latelet aggregation (20+/-4%), and blood viscosity (1.6+/-0.2 centipoi s, P < 0.01), and increased leg blood flow (97+/-16 ml/min), heart rat e, and plasma catecholamine levels (P < 0.01). In study II, plasma ins ulin levels remained suppressed at baseline; in this condition, the va scular responses to L-arginine were significantly reduced, except for plasma catecholamines which did not change significantly. In study III , the plasma insulin response to L-arginine was reestablished: this wa s associated with hemodynamic and theologic changes following L-argini ne not significantly different from those recorded in study I. These f indings show that systemic infusion of L-arginine in healthy subjects induces vasodilation and inhibits platelet aggregation and blood visco sity. These effects are mediated, in part, by endogenous released insu lin.