期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 540, 期 3, 页码 907-919出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1113/jphysiol.2001.014803
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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.
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