Jones L M, Michell R H
Biochem J. 1974 Sep;142(3):583-90. doi: 10.1042/bj1420583.
When rat parotid fragments that had been labelled with (32)P in vivo were exposed to high concentrations of acetylcholine, radioactivity was lost from phosphatidylinositol but not from other phospholipids. Simultaneously the concentration of phosphatidylinositol in the tissue decreased. If previously unlabelled tissue was incubated with (32)P(i) an increase in incorporation of radioactivity into phosphatidylinositol 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's phosphatidylinositol disappearing within 5min. Similar effects were evoked by stimulation with methacholine and by high concentrations of tetramethylammonium 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 phosphorylinositol group from the molecule; this is mediated through muscarinic cholinergic receptors. This is followed by a compensatory increase in the rate of synthesis of phosphatidylinositol, 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 phosphatidylinositol turnover.
当在体内用（32）P标记的大鼠腮腺碎片暴露于高浓度乙酰胆碱时，放射性从磷脂酰肌醇中丢失，但其他磷脂未丢失。同时，组织中磷脂酰肌醇的浓度降低。如果将先前未标记的组织与（32）P（i）一起孵育，则在浓度降低期间观察到放射性掺入磷脂酰肌醇的增加。乙酰胆碱的作用被阿托品阻断，但不被筒箭毒碱阻断。对乙酰胆碱的反应迅速，在5分钟内组织中高达三分之一的磷脂酰肌醇消失。用醋甲胆碱刺激和高浓度的四甲基铵离子也能引起类似的作用；这些反应也对阿托品敏感而对筒箭毒碱不敏感。得出的结论是，受乙酰胆碱刺激影响的肌醇脂质代谢事件是从分子中去除磷酸肌醇基团；这是通过毒蕈碱胆碱能受体介导的。随后是磷脂酰肌醇合成速率的代偿性增加，这在过去已有详细描述。将这些观察结果与以前研究人员的结果进行了比较，并结合与刺激引起的磷脂酰肌醇周转意义相关的现有假说进行了讨论。
