Requirement for calcium ions in acetylcholine-stimulated phosphodiesteratic cleavage of phosphatidyl-myo-inositol 4,5-bisphosphate in rabbit iris smooth muscle.
Requirement for calcium ions in acetylcholine-stimulated phosphodiesteratic cleavage of phosphatidyl-myo-inositol 4,5-bisphosphate in rabbit iris smooth muscle.
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兔虹膜平滑肌中乙酰胆碱刺激的磷脂酰肌醇 4,5-二磷酸酯的磷酸二酯裂解对钙离子的需求。
DOI：
10.1042/bj1920783
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Abdel-Latif,AA
中科院分区：
文献类型：
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作者：
Akhtar,RA;Abdel-Latif,AA
1.本文研究了乙酰胆碱刺激兔虹膜平滑肌磷脂酰肌醇4，5-二磷酸的分解及其对细胞外Ca ~（2+）依赖性的机制。2.乙酰胆碱（50μm）使[3 H]肌醇标记的肌肉中磷脂酰肌醇二磷酸的分解增加了28%，磷脂酰肌醇的标记增加了24%。在相同的实验条件下，3 H标记的三磷酸肌醇和一磷酸肌醇的产量分别增加了33%和48%。类似地，氨基甲酰胆碱和离子载体A23187增加了这些水溶性肌醇磷酸盐的产生。肌醇二磷酸的~ 3 H放射性变化不大。3.肌醇三磷酸酶和肌醇单磷酸酶均存在于该组织的亚细胞组分中，前者的比活性比后者高几倍。4.阿托品（20μm）可抑制乙酰胆碱刺激的三磷酸肌醇和单磷酸肌醇的产生，而筒箭毒碱（100μm）则无此作用; EGTA耗竭细胞外Ca ~（2+）可消除此作用，但加入低浓度Ca ~（2+）（20μm）可恢复此作用。5.钙拮抗剂如维拉帕米（20μm）、二苯丁胺（20μm）或镧（2 mm）也能抑制乙酰胆碱诱导的水溶性磷酸肌醇的产生。6.在50μ m-Ca ~（2+）存在下，43%的Ca ~（2+）刺激虹膜肌微粒体组分（“微粒体”）从外源性磷脂酰肌醇二磷酸释放三磷酸肌醇。7.结果表明，乙酰胆碱和离子载体A23187能显著激活磷酸肌醇二磷酸磷酸二酯酶，增加三磷酸肌醇及其水解产物单磷酸肌醇的生成。观察到的肌醇单磷酸生产的显着增加也可能是由于钙激活磷脂酰肌醇磷酸二酯酶。然而，这种磷脂的3 H放射性并没有随之降低。
1. The mechanism of acetylcholine-stimulated breakdown of phosphatidyl-myo-inositol 4,5-bisphosphate and its dependence on extracellular Ca2+was investigated in the rabbit iris smooth muscle. 2. Acetylcholine (50μm) increased the breakdown of phosphatidylinositol bisphosphate in [3H]inositol-labelled muscle by 28% and the labelling of phosphatidylinositol by 24% of that of the control. Under the same experimental conditions there was a 33 and 48% increase in the production of3H-labelled inositol trisphosphate and inositol monophosphate respectively. Similarly carbamoylcholine and ionophore A23187 increased the production of these water-soluble inositol phosphates. Little change was observed in the3H radioactivity of inositol bisphosphate. 3. Both inositol trisphosphatase and inositol monophosphatase were demonstrated in subcellular fractions of this tissue and the specific activity of the former was severalfold higher than that of the latter. 4. The acetylcholine-stimulated production of inositol trisphosphate and inositol monophosphate was inhibited by atropine (20μm), but not tubocurarine (100μm); and it was abolished by depletion of extracellular Ca2+with EGTA, but restored on addition of low concentrations of Ca2+(20μm). 5. Calcium-antagonistic agents, such as verapamil (20μm), dibenamine (20μm) or La3+(2mm), also abolished the production of the water-soluble inositol phosphates in response to acetylcholine. 6. Release of inositol trisphosphate from exogenous phosphatidylinositol bisphosphate by iris muscle microsomal fraction (‘microsomes’) was stimulated by 43% in the presence of 50μm-Ca2+. 7. The results indicate that increased Ca2+influx into the iris smooth muscle by acetylcholine and ionophore A23187 markedly activates phosphatidylinositol bisphosphate phosphodiesterase and subsequently increases the production of inositol trisphosphate and its hydrolytic product inositol monophosphate. The marked increase observed in the production of inositol monophosphate could also result from Ca2+activation of phosphatidylinositol phosphodiesterase. However, there was no concomitant decrease in the3H radioactivity of this phospholipid.