Inositol 1,4,5-trisphosphate releases Ca²⁺ from intracellular store sites in skinned single cells of porcine coronary artery

Effects of inositol 1,4,5-trisphosphate, extracted from human erythrocyte ghosts, on Ca²⁺ 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 Ca²⁺ from the intracellular non-mitochondrial store sites, within 1 min. However, when the concentrations of free Ca²⁺ were over 1.5 × 10^-6 M, the release of Ca²⁺ by this agent was inhibited. The Ca²⁺ releasing mechanism differed from that seen with A23187, therefore this release of Ca²⁺ from store sites was not due to Ca²⁺ ionophore actions. This agent may play the role of messenger in increasing the cytosolic Ca²⁺, provoking pharmacomechanical coupling, and thus producing the contraction.