Inhibition by ca 2+ of the incorporation of myo-inositol into phosphatidylinositol

Abstract

The incorporation of myo-[2- 3H]inositol into phosphatidylinositol of the aorta and the vas deferens was measured and the effects of Ca 2+ and other divalent cations were determined. When incubated in normal Krebs-Ringer buffer, only negligible radioactivity was incorporated into aorta slices. Mn 2+ increased the incorporation greatly. The enhanced incorporation was attributable to an increase in CDP-diglyceride:inositol transferase activity, rather than the myo-inositol exchange reaction. Transferase activity was increased 20-fold by 1 mM Mn 2+, in the presence of 20 mM Mg 2+. The Mn 2+-stimulated activity was strongly inhibited by Ca 2+. In the absence of Mn 2+, but presence of 20 mM Mg 2+, transferase activity was inhibited 80% by 0.01 mM Ca 2+. Removal of endogenous Ca 2+ from the tissue by ionophore A23187 and EGTA increased the incorporation of myo-[2- 3H]inositol into phosphatidylinositol. These findings indicate that Ca 2+ inhibited the synthesis of phosphatidylinositol. The proposed action of cholinergic and α-adrenergic agonists in enhancing the degradation and turnover of phosphatidylinositol and in provoking the influx of Ca 2+ should be unfavorable to the recovery of cellular phosphatidylinositol content.