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Cardiovascular Research 2003 60(3):457-459; doi:10.1016/j.cardiores.2003.10.005
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Shear stress and intermediate-conductance calcium-activated potassium channels

Ed van Bavel*

Department of Medical Physics, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands

*Tel.: +31-20-5665203; fax: +31-20-6917233. Email address: e.vanbavel@amc.uva.nl

Received 29 September 2003; accepted 6 October 2003

The first 10% of the full text of this article appears below.

See article by Brakemeier et al. [4] (pages 488–496) in this issue.


   1. Introduction
 
Vascular endothelial cells (EC) are continuously exposed to shear stress associated with the flowing blood. Over the years, it has become clear that such shear exerts a multitude of effects on endothelial biology and vascular function and structure, ranging in time span from seconds to months. On the scale of seconds, shear-dependent vasodilation has been demonstrated in many experimental settings. In the course of months, shear stress is believed to shape the vascular bed through remodeling [1]. Thus, shear stress sensing provides a mechanistic base for the notion of Murray in 1926 that vascular . . . [Full Text of this Article]


   2. Intermediate-conductance calcium-activated potassium (IKCa) channels in EC
 

   3. Upregulation of IKCa channels by shear stress
 

   4. Role of IKCa channels in endothelium-dependent dilation
 

   5. HUVECS as models for shear stress studies
 

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