Molecular Pharmacology, Vol 11, 79-86, Copyright © 1975 by the American Society for Pharmacology and Experimental Therapeutics

Incorporation of Inorganic [³²P]Phosphate into Rat Parotid Phosphatidylinositol

Induction through Activation of Alpha Adrenergic and Cholinergic Receptors and Relation to K⁺ Release

¹ Department of Biological Chemistry, The Hebrew University of Jerusalem, Jerusalem, Israel

Epinephrine and carbamylcholine, which cause K⁺ release in rat parotid slices, also increase the incorporation of ³²P_i into phosphatidylinositol. The effects of epinephrine on K⁺ release and ³²P_i incorporation were inhibited by phentolamine but not by atropine, whereas the effects of carbamylcholine were inhibited by atropine but not by phentolamine. Epinephrine at 20 µM caused a half-maximal increase in the incorporation of ³²P_i into phosphatidylinositol; this is similar to the value previously determined for the alpha adrenergic response of K⁺ release. Induction of massive enzyme secretion by isoproterenol of N⁶,O²'-dibutyryladenosine 3',5'-monophosphate (dibutyryl cyclic AMP) had no effect on the incorporation of ³²P_i. No changes in the composition of the major phospholipids of the parotid gland were observed. The epinephrine-induced K⁺ release was dependent upon calcium and reached a steady state within 5 min. On the other hand, the increased incorporation of ³²P_i into phosphatidylinositol showed a lag of about 10 min, was inhibited by Ca²⁺, and was maximally increased in the presence of ethylene glycol bis(-aminoethyl ether)-N,N'-tetraacetic acid. It is concluded that the K⁺ release is neither a prerequisite for nor the direct result of the increased incorporation of ³²P_i into phosphatidylinositol.