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Circulation Research
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Circulation Research. 2004;94:271-272
doi: 10.1161/01.RES.0000119803.07796.CA
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(Circulation Research. 2004;94:271.)
© 2004 American Heart Association, Inc.


Editorials

Tied Down by Shear Force

Role for Tie1 in Postnatal Vascular Remodeling?

Duncan J. Stewart, B. Lowell Langille

From the Terrence Donnelly Research Laboratories (D.J.S.), Division of Cardiology, St Michael’s Hospital, and the Department of Medicine, University of Toronto; Department of Laboratory Medicine and Pathobiology (D.J.S., B.L.L.), University of Toronto, Toronto, Ontario, Canada.

Correspondence to Duncan J. Stewart, Dexter Hung-Cho Man Chair and Head of the Division of Cardiology, St Michael’s Hospital, 30 Bond St, Suite 7-081 Queen Wing, Toronto, Ontario, Canada, M5B 1W8. E-mail stewartd@smh.toronto.on.ca


Key Words: shear force • arterial remodeling • postnatal vascular function


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

Shear forces play an important role in the regulation of vascular function and structure. Since the initial demonstration of flow-dependent dilation, the critical role of the endothelium in sensing changes in intimal shear stress, and transducing these into changes in vascular tone, has been well recognized.1–3 The moment-to-moment adjustments in arterial diameter involve the release of endothelial-derived vasoactive factors, in particular NO, and play a central role in optimizing the conductance of the large arterial tree and maintaining peak efficiency of the circulation even when subjected to profound changes in blood flow.4 However, the mechanisms governing the longer-term adaptations of vascular diameter and branching are equally or even more important for ensuring the appropriate development, patterning, and structure of the arterial tree, but they have not been well characterized. Here, too, the endothelium plays a pivotal role in adapting the diameter of an artery to persistent changes in flow,5 in this case by structural changes in the medial layers, rather than just vasomotion.6 Although it is likely that endothelial-derived vasoactive factors such as NO7 also play an important role in this process as well, the full cast of mediators of arterial remodeling remains to be defined.

It is perhaps not surprising that many of the same factors that mediate angiogenesis during blood vessel development may contribute to the remodeling of blood vessels in response to changing flow conditions and vice versa. For example, endothelium-derived NO, the classical mediator of shear-induced changes in vascular diameter, has recently been recognized as an . . . [Full Text of this Article]




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A. R. Pries, B. Reglin, and T. W. Secomb
Remodeling of Blood Vessels: Responses of Diameter and Wall Thickness to Hemodynamic and Metabolic Stimuli
Hypertension, October 1, 2005; 46(4): 725 - 731.
[Abstract] [Full Text] [PDF]