Abstract

Effects of inositol 1,4,5-trisphosphate, extracted from human erythrocyte ghosts, on Ca 2+ release from intracellular store sites were studied in saponin-treated single muscle cells of the porcine coronary artery. Application of micromolar concentrations of inositol 1,4,5-trisphosphate released Ca 2+ from the intracellular non-mitochondrial store sites, within 1 min. However, when the concentrations of free Ca 2+ were over 1.5 × 10 −6 M, the release of Ca 2+ by this agent was inhibited. The Ca 2+ releasing mechanism differed from that seen with A23187, therefore this release of Ca 2+ from store sites was not due to Ca 2+ ionophore actions. This agent may play the role of messenger in increasing the cytosolic Ca 2+, provoking pharmacomechanical coupling, and thus producing the contraction.

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