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(Circulation. 1996;94:1197-1198.)
© 1996 American Heart Association, Inc.

Articles

Nitric Oxide and Hypertension

Nigel Benjamin, DM; John Vane, FRS

St. Bartholomew's and The Royal London School of Medicine and Dentistry (N.B.) and the William Harvey Institute, London, England.

Correspondence to Nigel Benjamin, DM, St. Bartholomew's and The Royal London School of Medicine and Dentistry, West Smithfield, London, UK EC1A 7BE.

Key Words: Editorials • hypertension • endothelium • vasodilation • acetylcholine

	Introduction

 
In this issue, Taddei and colleagues¹ present evidence that offspring of hypertensive parents show a reduced forearm dilator response to local (brachial artery) infusion of acetylcholine, with the implication that endothelial nitric oxide synthesis is impaired in these subjects. This study follows from a number of related studies in the past few years.

Acetylcholine induces vasodilation through the release of endothelium-derived relaxing factor in vitro,² identified in endothelial cells in culture as nitric oxide, a potent vasodilator molecule.³ It is clearly of interest to ask whether human hypertension is caused by a defect in endothelial nitric oxide synthesis or by an impaired vascular response to nitric oxide. The seminal study by Vallance and colleagues⁴ that showed that the forearm arterial circulation continually releases nitric oxide and the observation that nitric oxide prevents platelet activation⁵ and modifies vascular smooth muscle proliferation⁶ make this question even more important, for hypertension is strongly associated with vascular hypertrophy and occlusive vascular disease.

The problem is, How do we best measure nitric oxide synthesis in human vascular endothelium? This tissue synthesizes nitric oxide from L-arginine using a distinct enzyme that is constitutively active and further activated by endothelial shear stress. After synthesis, some nitric oxide will rapidly diffuse to underlying vascular smooth muscle (nitric oxide is a lipid- and water-soluble gas), while that released into the lumen is rapidly oxidized by superoxide anions (to peroxynitrite and then nitrate) and the hem of hemoglobin (to form nitrate and methemoglobin). Although direct measurement of nitric oxide from . . . [Full Text of this Article]

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