The role of Ca
++ mobilization from storage sites on the prostacyclin (PGI
2) generation was investigated utilizing saponized human umbilical vein endothelial cells (HUVEC). Bradykinin and thrombin increased PGI
2 generation, Inositol 1, 4, 5-trisphosphate (IP
3) formation and cytosolic free Ca
++ concentration ([Ca
++]
i). And these increases induced by bradykinin or thrombin were not observed in Ca
++ free solution, while their basal levels were maintained (Fig. 4, 6, 7). IP
3 increased
45Ca release from the storage sites in saponized HUVEC, and it was 35.7% of Ca ionophore releasable
45Ca. Its increase was not influenced by the pretreatment of antimycin and oligomycin (Fig. 8). Through these results it was concluded that; 1) The extracellular Ca
++ was not required for the maintenance of basal PGI
2 generation. 2) The enhancement of PGI
2 generation induced by bradykinin or thrombin was brought about from the increase of [Ca
++]
i, which was induced by the enhanced Ca
++ influx from the extracellular space and by the Ca
++ release from the storage sites triggered by IP
3 generation. 3) The first direct evidence was shown that IP
3 enhanced Ca
++ release from the non-mitochondrial storage sites in HUVEC, and the amount was 35.7% of Ca ionophore releasable Ca
++.
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