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Am J Physiol Heart Circ Physiol (August 15, 2002). doi:10.1152/ajpheart.00605.2002
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Articles in PresS, published online ahead of print August 15, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00605.2002
Submitted on July 24, 2002
Accepted on August 8, 2002

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

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

1 Biological Sciences, Plattsburgh State University, Plattsburgh, NY, USA
2 Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
3 Pharmacology, The University of Vermont, Burlington, VT, USA

* To whom correspondence should be addressed. E-mail: jbrayden{at}zoo.uvm.edu.

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 activation of cation channels. Here we show that activation of these vascular cation channels and pressure-induced depolarization are mediated by protein kinase C in cerebral resistance arteries. Diacyglycerol, phorbol myristate acetate, and cell-swelling activate a cation current that we have previously shown is mediated by transient receptor potential (TRP) channels. These currents, as well as the smooth muscle depolarization of intact arteries in response to 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.




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