Signal transduction mechanisms operated via receptor activation in the smooth muscle

本研究利用膜片钳技术研究了碳碱和组胺对豚鼠回肠单个平滑肌细胞膜电流的影响，以及对同一肠子的β -松香皮平滑肌张力的影响，试图阐明高毒碱受体或组胺受体刺激所带来的阳离子通道激活和Ca^<2+>储存释放的信号转导系统。组胺引起的阳离子电流和Ca^<2+>-store释放在药理学性质上与苯酚引起的没有区别。g蛋白系统在两种细胞对受体刺激的反应中发挥作用，但参与Ca^<2+>储存释放的g蛋白的特征是对百日咳毒素不敏感。这两种受体激动剂都作用于咖啡因敏感储存，通过形成三磷酸肌醇（IP3）释放Ca^<2+>。由于Ca^<2+>储存的释放，细胞质中Ca^<2+>的升高增强了响应受体刺激的阳离子电流。阳离子电流振荡的产生可能涉及Ca^<2+>存储的周期性释放，这是由受体刺激过程中形成的IP3触发的。

The present study was to investigate the effects of carbachol and histamine on membrane currents in single smooth muscle cells of guinea-pig ileum using a patch-clamp technique and on tension in beta -escin-skinned smooth muscle of the same intesitine, in an attempt to elucidate signal transduction systems involved in both activation of cationic channels and release of Ca^<2+> stores brought about by stimulation of eigher muscarinic or histamine receptors.1. Both cationic current and Ca^<2+>-store release elicited by histamine are indistinguishable in pharmacological properties from those elicited by carbachol.2. A G-protein system plays a role in each of the two cellular responses to either receptor stimulation, but a G-protein involved in the release of Ca^<2+> stores is characterized by insensitivity to pertussis toxin.3. Both receptor agonists act on caffeine-sensitive stores to release Ca^<2+> via formation of inositol trisphosphate (IP3).4. The cationic current in response to receptor stimulation is potentiated by a rise in cytosolic Ca^<2+> due to release of Ca^<2+> stores. Generation of oscillations in the cationic current may involve cyclical release of Ca^<2+> stores which is triggerd by IP3 formed during receptor stimulation.