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J Physiol Volume 540, Number 3, 907-919, May 1, 2002 DOI: 10.1113/jphysiol.2001.014803
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Journal of Physiology (2002), 540.3, pp. 907-919
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2001.014803

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

G. D. S. Hirst, N. J. Bramich, N. Teramoto*, H. Suzuki† and F. R. Edwards

Department of Zoology, University of Melbourne, Victoria 3010, Australia, *Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan and †Department of Physiology, Medical School, Nagoya City University, Mizuho-ku, Nagoya 467, Japan

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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