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Regenerative component of slow waves in the guinea-pig gastric antrum involves a delayed increase in [Ca2+]i and Cl− channels

机译:豚鼠胃窦中慢波的再生成分涉及[Ca2 +] i和Cl-通道的延迟增加

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摘要

Regenerative potentials were initiated by depolarizing short segments of single bundles of circular muscle isolated from the gastric antrum of guinea-pigs. When changes in [Ca2+]i and membrane potential were recorded simultaneously, regenerative potentials were found to be associated with an increase in [Ca2+]i, with the increase starting after a minimum latency of about 1 s. Although the increase in [Ca2+]i was reduced by nifedipine, the amplitudes of the regenerative responses were little changed. Regenerative responses and associated changes in [Ca2+]i were abolished by loading the preparations with the Ca2+ chelator MAPTA-AM. Regenerative potentials were abolished by 2-aminoethoxydiphenyl borate (2APB), an inhibitor of IP3 induced Ca2+ release, by N-ethylamaleimide (NEM), an alkylating agent which blocks activation of G-proteins and were reduced in amplitude by two agents which block chloride (Cl−)-selective channels in many tissues. The observations suggest that membrane depolarization triggers IP3 formation. This causes Ca2+ release from intracellular stores which activates Ca2+-dependent Cl− channels.
机译:再生潜力是通过使从豚鼠胃窦腔中分离出的单束环形肌的短段去极化而开始的。当同时记录[Ca2 +] i和膜电位的变化时,发现再生电位与[Ca2 +] i的增加有关,并且在大约1 s的最小等待时间后开始增加。尽管硝苯地平减少了[Ca2 +] i的增加,但再生反应的幅度几乎没有变化。通过用Ca2 +螯合剂MAPTA-AM加载制剂,消除了[Ca2 +] i的再生反应和相关变化。再生电位被IP3-诱导的Ca2 +释放抑制剂2-氨基乙氧基二苯基硼酸酯(2APB),N-乙基NE丙啶(NEM)消除,后者是一种阻止G蛋白活化的烷基化剂,并被两种阻止氯化物的试剂降低了振幅许多组织中的(Cl-)选择通道。观察结果表明,膜去极化会触发IP3的形成。这会导致Ca2 +从细胞内存储释放,从而激活依赖Ca2 +的Cl-通道。

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