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Am J Physiol Heart Circ Physiol 277: H2264-H2271, 1999;
0363-6135/99 $5.00
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Vol. 277, Issue 6, H2264-H2271, December 1999

Integrin signaling, free radicals, and tyrosine kinase mediate flow constriction in isolated cerebral arteries

Jane A. Madden1,2 and Norbert J. T. Christman2

1 Department of Neurology, The Medical College of Wisconsin, Milwaukee 53226; and 2 Research Service, Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295

Isolated, cannulated, and pressurized (100 mmHg) middle cerebral arteries from adult cats were perfused intraluminally at rates from 0 to 4 ml/min with heated and gassed physiological saline solution. An electronic system held pressure constant by changing outflow resistance. The arteries constricted 18.1 ± 0.95% in response to flow and depolarized from -54 ± 0.51 to -40 ± 1.26 mV (P < 0.05). Constriction was independent of a functional endothelium but was eliminated by superoxide dismutase or tyrosine kinase inhibitors. Luminal perfusion with a synthetic extracellular matrix Arg-Gly-ASP (RGD) peptide that binds with integrin significantly reduced constriction to flow. Neither reducing intraluminal pressure nor increasing tone or shear stresses altered constriction to flow. Flow-induced constriction did not impede the ability of the arteries to dilate to hypercapnia, and inhibiting flow-induced constriction did not alter contractile responses to other agonists. These data suggest that, in vitro, middle cerebral arteries constrict to flow through a mechanism involving free radicals and tyrosine kinase and that flow shear stresses resulting in constriction are transduced by integrin signaling.

integrins; membrane potential


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