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(Hypertension. 2007;49:1.)
© 2007 American Heart Association, Inc.

Hypertension Highlights

Integrins, Vascular Remodeling, and Hypertension

From the Division of Cardiovascular and Endocrine Sciences, Faculty of Medical and Human Sciences, University of Manchester, United Kingdom.

Correspondence to Anthony M. Heagerty, Division of Cardiovascular and Endocrine Sciences, Faculty of Medical and Human Sciences, University of Manchester, Core Technology Facility, 46 Grafton St, Manchester, M13 9NT United Kingdom. E-mail tony.heagerty@manchester.ac.uk

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

	Introduction

 
At the level of the resistance artery, hypertension also brings about a thickening of the vascular wall and inward encroachment on the lumen. This has been reported as being attributable to hypertrophy or hyperplasia of vascular smooth muscle cells (VSMCs), but studies have appeared suggesting that growth is not apparent in arteries at this level of the circulation.¹ In addition, detailed structural and mechanical analyses have shown that eutrophic inward remodeling can narrow the vascular lumen without precipitating hypertrophy.^2,3 A small amount of hypertrophy may be observed, and in some pathological states, hypertrophy may supervene and is an adverse prognostic sign.⁴ For the remainder of this section, we consider the reasons why resistance arteries respond to hypertension in this manner.

To understand how hypertension produces the above nonhypertrophic changes in small arteries, one must look at the role of the resistance vasculature. At physiological pressures, these vessels typically exhibit a level of contraction (myogenic tone) independent of neurohormonal influences. This response enables blood vessels to constrict or dilate in response to changes in pressure. This process, known as the myogenic response, is only observed in smaller resistance arteries, which mediate autoregulation of blood flow and stabilize capillary pressure.⁵

Hypertrophy is observed in vessels that do not possess myogenic tone, whereas, in smaller resistance arteries, an initial increase in pressure will bring about increased myogenic constriction, which, if prolonged, will lead to inward eutrophic remodeling and/or a reduced arterial distensibility.⁶ This structural difference between large conduit and resistance arteries is apparent . . . [Full Text of this Article]

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