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Correspondence
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Volume 328:287-288 January 28, 1993 Number 4
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Effect of L-Arginine on Plasminogen-Activator Inhibitor in Hypertensive Patients with Hypercholesterolemia

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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 hypertension1. Indeed, exogenous L-arginine produces systemic hypotension in patients with essential hypertension2.

Sodium nitroprusside (a nitric oxide donor) inhibits the release of plasminogen-activator inhibitor (PAI) from platelets and has fibrinolytic properties3. Plasma PAI activity is increased in patients with hypertension, venous thrombosis, and recurrent myocardial infarction4.

L-Arginine hydrochloride (Boehringer-Mannheim), at a daily dose of 60 mmol given over a three-hour period, . . . [Full Text of this Article]

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