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In experiments performed on digitonin-treated myometrium cells the existence of intracellular energy-dependent Ca(2+)-transporting system has been identified. The mitochondria-linked energy-dependent accumulation of Ca2+ was inhibited by ruthenium red and sodium azide with Ki of 0.7 +/- 0.3 microM and 1.1 +/- 0.4 mM, respectively. The Ca2+ ionophore A23187 added to the incubation medium following the termination of the accumulation process by ruthenium red caused a discharge of Ca2+ accumulated from the mitochondria. In the endoplasmic reticulum there exists a Mg2+,ATP-dependent Ca(2+)-pump which is potentiated by oxalate, immune to ruthenium red and sodium azide and inhibited by thapsigargin with Ki < 20 nM. In the absence of oxalate, the component of mitochondrial accumulation of Ca2+ was 3-4 times higher that of the endoplasmic reticulum. These results indicate that under the conditions used the calcium capacity of mitochondria was significantly higher than that of the endoplasmic reticulum. It is suggested that mitochondria serve as a high capacity intracellular Ca(2+)-accumulating store protecting smooth muscle cells from Ca2+ overload under some abnormal states. Under normal physiological conditions the endoplasmic reticulum serves as the major intracellular store involved in the pharmacomechanical coupling in the smooth muscle of the myometrium.


Journal article



Publication Date





1218 - 1229


Adenosine Triphosphate, Animals, Azides, Calcimycin, Calcium, Endoplasmic Reticulum, Energy Metabolism, Female, Mitochondria, Muscle, Myometrium, Rats, Ruthenium Red, Sodium Azide, Terpenes, Thapsigargin