Sanders K M, Publicover N G
Department of Physiology, University of Nevada School of Medicine, Reno 89511.
Dig Dis Sci. 1994 Dec;39(12 Suppl):69S-72S. doi: 10.1007/BF02300375.
Several mechanisms contribute to the regulation of force generated by gastric muscles. Phasic contractions in the stomach are triggered by the propagation of electrical slow waves. These events are associated with an influx of Ca2+ and an increase in intracellular Ca2+ sufficient to elicit contraction. Entry of Ca2+ may be supplemented by the release of Ca2+ from intracellular stores. Excitatory agonists enhance the amplitude of slow waves, increase the amplitude of Ca2+ transients, and increase the force of phasic contractions. Inhibitory agonists have opposite effects. Excitatory agonists may also enhance release of Ca2+ from stores via the production of IP3. Excitatory and inhibitory agonists may also regulate the sensitivity of the contractile apparatus for Ca2+ and therefore alter the contractile response to a given change in intracellular Ca2+.
有几种机制参与调节胃肌产生的力量。胃中的阶段性收缩由电慢波的传播引发。这些事件与Ca2+的内流以及细胞内Ca2+的增加有关,这种增加足以引发收缩。Ca2+的进入可能会因细胞内储存库释放Ca2+而得到补充。兴奋性激动剂会增强慢波的振幅,增加Ca2+瞬变的振幅,并增加阶段性收缩的力量。抑制性激动剂则有相反的作用。兴奋性激动剂还可能通过产生肌醇三磷酸(IP3)来增强Ca2+从储存库中的释放。兴奋性和抑制性激动剂也可能调节收缩装置对Ca2+的敏感性,从而改变对细胞内Ca2+给定变化的收缩反应。