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AJP - Heart and Circulatory Physiology, Vol 261, Issue 5 1464-H1470, Copyright © 1991 by American Physiological Society
ARTICLES |
K. Ito, T. Ikemoto and S. Takakura
Department of Veterinary Pharmacology, Faculty of Agriculture, Miyazaki University, Japan.
Application of Ca2+ (0.1-2.5 mM) to guinea pig aortas incubated in Ca(2+)-free isotonic KCl solution induced a contraction (Ca contraction), a part of which depended on preloading the intracellular stores with Ca2+ and which was sensitive to 3 x 10(-5) M ryanodine. Because 45Ca2+ influx from the external fluid upon the addition of Ca2+ was not modified either by the state of filling of the Ca2+ store or by the presence of ryanodine, the ryanodine-sensitive component of the contraction could be attributed to the Ca2+ influx-induced Ca2+ release from the Ca2+ store. Supporting the possibility of involvement of Ca(2+)-induced Ca2+ release, the Ca contraction due to 0.1 mM Ca2+ was enhanced either by decreasing Mg2+ in the medium or by low temperature. The ratio of the ryanodine-sensitive fraction in the Ca contraction was inversely related to the concentration of Ca2+ added and also to the extent of 45Ca2+ influx. When the Ca2+ influx was decreased by verapamil or cadmium, the ratio of ryanodine-sensitive fraction increased. On the contrary, an increase of Ca2+ influx by CGP-28392 decreased the ratio. These results suggest that Ca2+ influx at a physiological level triggers Ca2+ release from the Ca2+ store, resulting in the amplification of contractile force.
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