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Articles in PresS, published online ahead of print August 15, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00554.2002
Submitted on July 3, 2002
Accepted on August 9, 2002
1 Urology & Physiology & Biophysics, Albert Einstein College of Medicine, Bronx, New York, N.Y., USA
2 Physiology & Biophysics, University of British Columbia, Vancouver, BC, Canada
3 Pharmacology & Therapeutics, University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: laher{at}interchange.ubc.ca.
Pressure induced myogenic tone is accompanied by membrane depolarization and Ca2+ entry via voltage gated Ca2+ channels. Recent evidence also suggests that intracellular Ca2+-sensitization of the contractile proteins also occurs. Both PKC and Rho kinase are candidate second messengers for the mediation of the sensitization process. We investigated the signaling pathways of myogenic reactivity in rat cerebral arteries in vessels that were depolarized with a high potassium (K+) solution. Arteries were mounted in a pressure myograph and pressure-induced myogenic tone (PMT) was recorded. In some experiments simultaneous changes in intracellular Ca2+ concentration [Ca2+]i were recorded using fura-2 fluorescence photometry. Step increases of pressure induced contractions with significant changes in [Ca2+]i at high pressures (60-100 mm Hg). The ratio of force change to change in Ca2+ for was greater for myogenic tone compared to tone due to depolarization with 60KPSS, suggesting that in addition to increases in [Ca2+]i, increases in myofilament Ca2+ sensitivity occur during myogenic reactivity. .Membrane depolarization by high-K+ saline increased [Ca2+]i via a Ca2+ influx pathway insensitive to insensitive to PKC inhibition. Cerebral arteries were able to maintain their diameters in the continued presence of 60KSS. Pressure induced constriction under these conditions was not associated with further increases in Ca2+ but was abolished by selective inhibitors of PLC, PKC and Rho kinase. Our results suggest that in addition to increasing voltage gated Ca2+ influx, pressure induced changes in diameter are accompanied by increased myofilament sensitivity to calcium medicated by PKC/Rho kinase activation.
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