Incorporation of inorganic [³²P] phosphate into rat parotid phosphatidylinositol. Induction through activation of alpha adrenergic and cholinergic receptors and relation to K⁺ release

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. The increased incorporation of ³²P(i) into phosphatidylinositol showed a lag of about 10 min, was inhibited by Ca²⁺, and was maximally N,N' the presence of ethylene glycol bis(β 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.