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(Hypertension. 2007;50:204.)
© 2007 American Heart Association, Inc.

Sixth International Workshop on Structure and Function of the Vascular System

Microvascular Dysfunction

A Potential Pathophysiological Role in the Metabolic Syndrome

Erik H. Serné; Renate T. de Jongh; Etto C. Eringa; Richard G. IJzerman; Coen D.A. Stehouwer

From the Department of Internal Medicine (E.H.S., R.T.d.J., R.G.I.), VU Medical Center, Amsterdam; the Laboratory for Physiology (E.C.E.), Institute for Cardiovascular Research, VU Medical Center, Amsterdam; and the Department of Internal Medicine (C.D.A.S.), Academic Hospital Maastricht, The Netherlands.

Correspondence to Dr E.H. Serné, Department of Internal Medicine, VU Medical Center, PO Box 7057, 1007 MB Amsterdam, The Netherlands. E-mail e.serné@vumc.nl; or Prof Dr C.D.A. Stehouwer, Department of Internal Medicine, Academic Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands. E-mail csteh@sint.azm.nl

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

	Introduction

 
Obesity and a central body fat distribution, hypertension, insulin resistance, glucose intolerance, dyslipidemia, and proinflammatory and prothrombotic factors are all part of the metabolic syndrome. The metabolic syndrome defines a clustering of metabolic risk factors which confers an increased risk for type 2 diabetes and cardiovascular disease.¹ In the past years a large amount of research has been aimed at elucidating the pathophysiology underlying this clustering of risk factors, because a better understanding may lead to new therapeutic approaches that specifically target underlying causes of the metabolic syndrome.

Recently, it has become clear that microvascular dysfunction, by affecting both pressure and flow patterns, may have consequences not only for peripheral vascular resistance, but also for insulin-mediated changes in muscle perfusion and glucose metabolism, providing a novel pathophysiological framework for understanding the association between hypertension, obesity, and impaired insulin-mediated glucose disposal.^2–4

The present article examines recent data concerning the role of microvascular dysfunction as an explanation for the associations among hypertension, obesity, and impaired insulin-mediated glucose disposal.

	Description of the Microcirculation

 
An exact definition of the microcirculation is elusive. Morphologically, the microcirculation is widely taken to encompass vessels <150 µm in diameter. It therefore includes arterioles, capillaries, and venules. Alternatively, a definition based on arterial vessel physiology rather than diameter or structure has been proposed.³ By this definition, all arterial vessels that respond to increasing pressure by a myogenic reduction in lumen diameter are included in the microcirculation. Such a definition would include the smallest arteries and arterioles in the microcirculation in addition to capillaries . . . [Full Text of this Article]

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