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Am J Physiol Cell Physiol (November 21, 2001). doi:10.1152/ajpcell.00247.2001
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Articles in PresS, published online ahead of print November 20, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00247.2001
Submitted on June 4, 2001
Accepted on November 14, 2001

Dual effect of fluid shear stress on volume-regulated anion current in bovine aortic endothelial cells

Victor G Romanenko1, Peter F Davies1, and Irena Levitan1*

1 Institute for Medicine and Engineering, University of Pennsylvania, Philadelphia, PA, USA

* To whom correspondence should be addressed. E-mail: ilevitan{at}mail.med.upenn.edu.

The key mechanism responsible for maintaining cell volume homeostasis is activation of volume-regulated anion channels (VRAC). The role of hemodynamic shear stress in the regulation of VRAC in bovine aortic endothelial cells (BAECs) was investigated. We show that acute changes in shear stress have a biphasic effect on the development of VRAC. A shear stress step from a background flow (0.1 dyn/cm2) to 1 dyn/cm2 enhanced VRAC activation induced by an osmotic challenge. Flow alone, in the absence of osmotic stress, did not induce VRAC activation. Increasing the shear stress to 3 dyn/cm2, however, resulted only in a transient increase of VRAC activity followed by an inhibitory phase during which VRAC was gradually suppressed. When shear stress was increased further (5-10 dyn/cm2), the current was immediately strongly suppressed. Suppression of VRAC was observed both in cells challenged osmotically, as well as in cells that developed spontaneous VRAC under isotonic conditions. Our findings suggest that shear stress is an important factor in regulating the ability of vascular endothelial cells to maintain their volume homeostasis.




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