Effect of increased availability of endothelium-derived nitric oxide precursor on endothelium-dependent vascular relaxation in normal subjects and in patients with essential hypertension.

摘要: BACKGROUND Patients with essential hypertension have a deficit in the endothelium-derived nitric oxide system that results impaired endothelium-dependent vascular relaxation. The objective of this study was to determine whether abnormality is caused by deficiency substrate for synthesis. METHODS AND RESULTS responses acetylcholine (an vasodilator infused at 7.5, 15, and 30 micrograms/min) sodium nitroprusside (a direct smooth muscle dilator 0.8, 1.6, 3.2 were studied during combined administration dextrose 5% or L-arginine (substrate synthesis 40 mumol/min) 12 normal control subjects (seven men five women; age, 49.3 +/- 7 years) 14 hypertensive patients (nine 48.4 years). In addition, effect D-arginine (stereoisomer arginine not precursor oxide) on eight seven patients. Drugs into brachial artery, response forearm vasculature measured strain gauge plethysmography. significantly blunted compared (maximum flow, 8.9 5 versus 15.7 6 mL.min-1.100 mL-1, respectively; p CONCLUSIONS humans, availability production rate-limiting step contrast, increased does modify endothelium-mediated vasodilation These findings provide further evidence defect indicate related decreased production.