The Role of Endogenous Insulin

This study aimed at evaluating whether increased availability of the natural precursor of nitric oxide, L -arginine, could influence systemic hemodynamic and rheologic parameters in humans and whether the effects of L -arginine are mediated by endogenous insulin. 10 healthy young subjects participated in the following studies: study I, infusion of L -arginine (1 g/min for 30 min); study II, infusion of L -arginine plus octreotide (25 m g as i.v. bolus 1 0.5 m g/min) to block endogenous insulin and glucagon secretion, plus replacement of basal insulin and glucagon; study III, infusion of L -arginine plus octreotide plus basal glucagon plus an insulin infusion designed to mimic the insulin response of study I. L -Arginine infusion significantly reduced systolic (11 6 3, mean 6 SE) and diastolic (8 6 2 mmHg, P , 0.001) blood pressure, platelet aggregation (20 6 4%), and blood viscosity (1.6 6 0.2 centipois, P , 0.01), and increased leg blood flow (97 6 16 ml/min), heart rate, and plasma catecholamine levels ( P , 0.01). In study II, plasma insulin levels remained suppressed at baseline; in this condition, the vascular 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 was associated with hemodynamic and rheologic changes following L -arginine not significantly different from those recorded in study I. These findings show that systemic infusion of L -arginine in healthy subjects induces vasodilation and inhibits platelet aggregation and blood viscosity. These effects are mediated, in part, by endogenous released insulin. ( J. Clin. Invest . 1997. 99:433– 438.)