Effect of L-Arginine on Plasminogen-Activator Inhibitor in Hypertensive Patients with Hypercholesterolemia

To the Editor: Vascular endothelium converts L-arginine to nitric oxide. An increase in blood pressure after the inhibition of nitric oxide synthase suggests that a deficiency of nitric oxide may contribute to the pathogenesis of hypertension 1 . Indeed, exogenous L-arginine produces systemic hypotension in patients with essential hypertension 2 . Sodium nitroprusside (a nitric oxide donor) inhibits the release of plasminogen-activator inhibitor (PAI) from platelets and has fibrinolytic properties 3 . Plasma PAI activity is increased in patients with hypertension, venous thrombosis, and recurrent myocardial infarction 4 . L-Arginine hydrochloride (Boehringer-Mannheim), at a daily dose of 60 mmol given over a three-hour period, . . .