Abstract

1,2-Didecanoylglycerol (diC 10) is taken up by human platelets and sequentially converted to 1,2-didecanoyl-phosphatidic acid (PA 10) and 1,2-didecanoylphosphatidylinositol (PI 10). Agents that increase cyclic AMP in platelets, such as prostacyclin and forskolin, sequentially convert diC 10 to pa 10 and PI 10. They decrease formation of PA 10 with a parallel accumulation of PI 10. This might reflect an inhibition of phosphatidylinositol kinase.

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