Breakdown of phosphatidylinositol provoked by muscarinic cholinergic stimulation of rat parotid gland fragments

When rat parotid fragments that had been labeled with 32P in vivo were exposed to high concentrations of acetylcholine, radioactivity was lost from phosphatidyl inositol but not from other phospholipids. Simultaneously the concentration of phosphatidyl inositol in the tissue decreased. If previously unlabelled tissue was incubated with 32Pi an increase in incorporation of radioactivity into phosphatidyl inositol was observed during this decrease in concentration. The effects of acetylcholine were blocked by atropine, but not by tubocurarine. The response to acetylcholine was rapid with up to one third of the tissue phosphatidyl inositol disappearing within 5 min. Similar effects were evoked by stimulation with methacholine and by high concentrations of tetramethyl ammonium ion; these responses were also atropine sensitive and tubocurarine insensitive. It is concluded that the event in inositol lipid metabolism that is affected by acetylcholine stimulation is removal of the phosphoryl inositol group from the molecule; this is mediated through muscarinic cholinergic receptors. This is followed by a compensatory increase in the rate of synthesis of phosphatidyl inositol, which has been described in detail in the past. These observations are compared with those of previous workers and are discussed in relation to the existing hypotheses relating to the significance of stimulus provoked phosphatidyl inositol turnover.