Shimuta S I, Borges A C, Prioste R N, Paiva T B
Department of Biophysics, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP, Brazil.
Eur J Pharmacol. 1999 Feb 12;367(1):59-66. doi: 10.1016/s0014-2999(98)00919-4.
Ca2+ pathways activated by angiotensin II and carbachol were evaluated in the circular muscle of the guinea-pig ileum by recording mechanical and electrical activities. Transient contractions induced by angiotensin II were greatly reduced by Ca2+ removal from the medium whereas carbachol-induced responses were not significantly altered. Nifedipine had no effect on the responses to both agonists. A high concentration of tetrodotoxin (0.1 microM) inhibited angiotensin II-induced contractile responses without affecting the depolarization, whereas 1 mM Ni2+ inhibited the mechanical and electrical effects. Neither tetrodotoxin nor Ni2+ affected carbachol-induced effects. These results indicate that angiotensin II-induced phasic contractions depend on extracellular Ca2+ but not on voltage-dependent L-type Ca2+ channels. It is suggested that angiotensin II activates Ni2+-sensitive Na+ and non-specific cationic channels, whereas the responses to carbachol are dependent on receptor-activated Ca2+ release. Furthermore the different response of the longitudinal and circular muscles to the inhibitory effects of tetrodotoxin and Ni2+ on the angiotensin II- and carbachol-induced contractions indicates that these agonists exert their own myogenic effects on each layer and are able to trigger different Ca2+ mobilization pathways.
通过记录机械和电活动,在豚鼠回肠环形肌中评估了由血管紧张素II和卡巴胆碱激活的Ca2+途径。从培养基中去除Ca2+可大大降低血管紧张素II诱导的瞬时收缩,而卡巴胆碱诱导的反应没有明显改变。硝苯地平对两种激动剂的反应均无影响。高浓度的河豚毒素(0.1 microM)可抑制血管紧张素II诱导的收缩反应而不影响去极化,而1 mM Ni2+可抑制机械和电效应。河豚毒素和Ni2+均不影响卡巴胆碱诱导的效应。这些结果表明,血管紧张素II诱导的相性收缩依赖于细胞外Ca2+,而不依赖于电压依赖性L型Ca2+通道。提示血管紧张素II激活Ni2+敏感的Na+和非特异性阳离子通道,而对卡巴胆碱的反应依赖于受体激活的Ca2+释放。此外,纵肌和环肌对河豚毒素和Ni2+对血管紧张素II和卡巴胆碱诱导的收缩的抑制作用的不同反应表明,这些激动剂对每一层发挥其自身的肌源性作用,并能够触发不同的Ca2+动员途径。