腮腺腺泡细胞中受体控制的肌醇三磷酸形成的特性。
Properties of receptor-controlled inositol trisphosphate formation in parotid acinar cells.
作者信息
Aub D L, Putney J W
出版信息
Biochem J. 1985 Jan 1;225(1):263-6. doi: 10.1042/bj2250263.
Abstract
Activation of muscarinic receptors in rat parotid cells results in breakdown of polyphosphoinositides liberating inositol phosphates, including inositol trisphosphate. Formation of inositol trisphosphate appears independent of agonist-induced Ca2+ mobilization, since neither formation nor degradation of inositol trisphosphate are appreciably altered in low-calcium media, and elevation of cytosolic Ca2+ with a calcium ionophore does not cause an increase in cellular inositol trisphosphate. Further, activation of substance P receptors and alpha 1-adrenoreceptors, but not beta-adrenoreceptors, increases inositol trisphosphate formation. The dose-response curve for methacholine activation of inositol trisphosphate formation more closely approximates the curve for receptor occupancy than for Ca2+-activated K+ release. These results are all consistent with the suggestion that inositol trisphosphate could function as a second messenger linking receptor occupation to cellular Ca2+ mobilization.
摘要
毒蕈碱受体在大鼠腮腺细胞中的激活导致多磷酸肌醇分解，释放出肌醇磷酸，包括肌醇三磷酸。肌醇三磷酸的形成似乎与激动剂诱导的Ca2+动员无关，因为在低钙培养基中，肌醇三磷酸的形成和降解均未明显改变，并且用钙离子载体提高胞质Ca2+水平不会导致细胞内肌醇三磷酸增加。此外，P物质受体和α1-肾上腺素能受体而非β-肾上腺素能受体的激活会增加肌醇三磷酸的形成。与Ca2+激活的K+释放曲线相比，乙酰甲胆碱激活肌醇三磷酸形成的剂量反应曲线更接近受体占据曲线。这些结果均与肌醇三磷酸可作为将受体占据与细胞Ca2+动员联系起来的第二信使这一观点一致。
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