PHARMACOMECHANICAL COUPLING IN SMOOTH-MUSCLE MAY INVOLVE PHOSPHATIDYLINOSITOL METABOLISM
PHARMACOMECHANICAL COUPLING IN SMOOTH-MUSCLE MAY INVOLVE PHOSPHATIDYLINOSITOL METABOLISM
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DOI：
10.1073/pnas.81.21.6899
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发表时间：
1984-01-01
期刊：
影响因子：
--
通讯作者：
COBURN, RF
中科院分区：
文献类型：
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作者：
BARON, CB;CUNNINGHAM, M;COBURN, RF
犬气管肌的胆碱能收缩是一种主要利用膜电位独立机制来激活收缩蛋白（药物机械耦合）的收缩，与磷脂酰肌醇池的减少、磷脂酸和二酰甘油池的增加以及 32PO4 掺入磷脂酰肌醇的增加有关。这些变化发生在收缩过程和张力维持过程中，并且与膜去极化或胞质 Ca2+ 浓度的增加无关。磷脂酰肌醇周转可能是受体转导过程的一部分，控制受体操纵的 Ca2+ 通道或参与平滑肌药物机械耦合的其他膜电位独立机制。
Cholinergic contraction of canine trachealis muscle, a contraction that primarily utilizes membrane potential-independent mechanisms for activating contractile proteins (pharmacomechanical coupling), is associated with a decline in the phosphatidylinositol pool, an increase in the phosphatidic acid and diacylglycerol pools, and an increased incorporation of 32PO4 into phosphatidylinositol. These changes occur during development of the contraction and during maintenance of tension and are independent of membrane depolarization or increases in cytosolic Ca2+ concentration. Phosphatidylinositol turnover may be part of a receptor transduction process controlling receptor-operated Ca2+ channels or other membrane potential-independent mechanisms involved in pharmacomechanical coupling in smooth muscle.