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(Hypertension. 2002;40:e3.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Nitric Oxide and Regulation of Arterial Elasticity: Right Idea, Wrong Vascular Bed?

Department of Clinical Pharmacology, Addenbrooke’s Hospital, Cambridge, England, United Kingdom

David J. Webb

Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, Scotland, United Kingdom

John R. Cockcroft

Wales Heart Research Institute, University Hospital, Cardiff, Wales, United Kingdom, E-mail cockcroftjr@cf.ac.uk

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We were disappointed with the reply to our recent letter about the involvement of nitric oxide (NO) in the regulation of arterial stiffness.¹ Although we enjoyed the well-written and robust reply to the points we raised, we feel obliged to point out a number of factual inaccuracies that may lead to misinterpretation of the debate and to refocus the issue on several points they seem to misunderstand.

Although Kinlay et al agree with our contention that pulse wave velocity in the brachial artery changes little with age, they suggest that this is irrelevant to their recent findings that NO regulates several indices of brachial artery elasticity (including pulse wave velocity) in vivo. However, we would disagree, because the same group have previously published data demonstrating that aging progressively impairs endothelium-dependent vasodilatation in the forearm vascular bed.² Therefore, if, as they maintain, NO is important in regulating arterial elasticity in the arm, surely brachial artery elasticity should decrease with age. Indeed, we would be interested to know how the authors reconcile both sets of observations.

Kinlay et al also suggest that their own technique "is independent of blood flow, as it is a direct assessment of arterial distension." However, as the authors well know, shear stress is the main physiological stimulus to endothelial nitric oxide production in vivo. Therefore, any drug that reduces blood flow will reduce shear stress and, thus, nitric oxide production in the large arteries. This means that changes in blood flow could influence large artery stiffness indirectly . . . [Full Text of this Article]

Scott Kinlay; Peter Ganz; Mark A. Creager

Department of Medicine, Cardiovascular Division, Brigham and Women’s Hospital, Boston, Massachusetts, E-mail skinlay@rics.bwh.harvard.edu