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Am J Physiol Heart Circ Physiol 274: H1920-H1927, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 6, H1920-H1927, June 1998

Temperature and protein kinase C modulate myofilament Ca2+ sensitivity in pressurized rat cerebral arteries

Natalia I. Gokina and George Osol

Department of Obstetrics and Gynecology, The University of Vermont, College of Medicine, Burlington, Vermont 05405

The effects of pharmacological activation and inhibition of protein kinase C (PKC) and temperature on the relationship between cytoplasmic Ca2+ and lumen diameter were studied in pressurized (50 mmHg) rat posterior cerebral arteries permeabilized with alpha -toxin. Increasing Ca2+ concentrations (30 nM-10 µM, 22°C) induced stable, concentration-dependent constrictions with a half-maximal effective concentration (EC50) of 112 nM. The maximal constriction was 80% of baseline diameter and 157% of that during depolarization of nonpermeabilized vessels with 124 mM KCl. Elevation of temperature to 37°C increased the EC50 to 246 nM and enhanced the steepness of concentration-response curves. Exposure of permeabilized arteries to indolactam V, an activator of PKC, resulted in a significant myofilament Ca2+ sensitization (e.g., EC50 at 5 µM = 126 nM) without changing efficacy. The effects of calphostin C, a PKC inhibitor, on Ca2+ sensitivity were minimal; however, the amplitude of Ca2+-induced constrictions in both control and indolactam-treated arteries was suppressed in a concentration-dependent manner. Thus 1) temperature is an important variable in studies of arterial Ca2+ sensitivity, and 2) changes in PKC activity can significantly alter both myofilament sensitivity to and constrictor efficacy of cytosolic Ca2+.

alpha -toxin permeabilized arteries; (-)-indolactam V; calphostin C; calcium ion


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