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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:892.)
© 2005 American Heart Association, Inc.

Editorials

Making Up and Breaking Up

The Tortuous Ways of the Vascular Wall

Stéphanie Lehoux; Alain Tedgui

From the INSERM Centre de Recherche Cardiovasculaire Lariboisiere, Paris, France.

Correspondence to Stephanie Lehoux, PhD, INSERM CRC Lariboisiere, 41, Bd de la Chapelle, 75010 Paris, France. E-mail lehoux@larib.inserm.fr

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

The concept that blood pressure influences vessel wall composition and structure is well established. Any alterations in stretch (caused by changes in blood pressure) solicit counteracting radial and tangential forces, driving transformations in the vessel wall that aim to accommodate the new conditions and to ultimately restore basal levels of tensile stress.^1–3 Thus, when tensile stress increases because of a rise in arterial pressure, smooth muscle cell hypertrophy and collagen and elastin contents augment. Inversely, when the circumferential stress falls, the wall undergoes atrophy.^4,5

See page 957

Understanding how vessel wall remodeling occurs is valuable because it relies on the delicate balance between restructuralization and overcompensation. For instance, vascular accumulation of type I, III, and IV collagen in hypertensive patients⁶ and in animal models of hypertension^7,8 effectively counteracts the distending force of blood pressure, but at length it also results in increased vascular stiffness. Clinically, vascular stiffness translates to greater pulse wave velocity, which is an independent predictor of mortality in patients with end-stage renal failure, hypertension, and diabetes, as well as in older individuals.⁹ In this issue of Atherosclerosis, Thrombosis and Vascular Biology, Jackson et al¹⁰ show that the opposite holds true for vessels in which axial tension is off-loaded. In rabbit carotid arteries elongated by interposition of the contralateral carotid artery, the authors found that tortuosity caused by loss of axial strain was not rectified in the months that followed the intervention. Smooth muscle cell proliferation was observed, but this was offset by equivalent cell apoptosis. Likewise, . . . [Full Text of this Article]

Related Article:

Partial Off-Loading of Longitudinal Tension Induces Arterial Tortuosity

Zane S. Jackson, Dorota Dajnowiec, Avrum I. Gotlieb, and B. Lowell Langille
Arterioscler Thromb Vasc Biol 2005 25: 957-962. [Abstract] [Full Text] [PDF]

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