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

Y. Oron, M. Loewe, Z. Selinger

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)79-86
Number of pages8
JournalMolecular Pharmacology
Volume11
Issue number1
StatePublished - 1975
Externally publishedYes

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