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Am J Physiol Heart Circ Physiol 283: H2196-H2201, 2002. First published August 15, 2002; doi:10.1152/ajpheart.00605.2002
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Vol. 283, Issue 6, H2196-H2201, December 2002

SPECIAL TOPICS
Diacylglycerol and protein kinase C activate cation channels involved in myogenic tone

Donald F. Slish1, Donald G. Welsh2, and Joseph E. Brayden3

1 Department of Biological Science, Plattsburgh State University, Plattsburgh, New York 12901; 2 Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and 3 Department of Pharmacology, University of Vermont, Burlington, Vermont 05405

The smooth muscle cells of resistance arteries depolarize and contract when intravascular pressure is elevated. This is a central characteristic of myogenic tone, which plays an important role in regulation of blood flow in many vascular beds. Pressure-induced vascular smooth muscle depolarization depends in part on the activation of cation channels. Here, we show that activation of these smooth muscle cation channels and pressure-induced depolarization are mediated by protein kinase C in cerebral resistance arteries. Diacylglycerol, phorbol myristate acetate, and cell swelling activate a cation current that we have previously shown is mediated by transient receptor potential channels. These currents, as well as the smooth muscle cell depolarizations of intact arteries induced by diacylglycerol, phorbol ester, and elevation of intravascular pressure, are nearly eliminated by protein kinase C inhibitors. These results suggest a major mechanism of myogenic tone involves mechanotransduction through phospholipase C, diacylglycerol production, and protein kinase C activation, which increase cation channel activity. The associated depolarization activates L-type calcium channels, leading to increased intracellular calcium and vasoconstriction.

pressure-induced depolarization; signal transduction; mechanotransduction


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