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Received September 19, 2001
Accepted after revision January 16, 2002
1 Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan
* To whom correspondence should be addressed. E-mail: hisuzuki{at}med.nagoya-cu.ac.jp.
Spontaneous electrical activity and internal Ca2+ concentration ([Ca2+]i) were measured simultaneously using conventional microelectrodes and fura-2 fluorescence, respectively, in isolated circular smooth muscle bundles of the guinea-pig gastric antrum. The smooth muscle bundles generated periodic slow potentials with accompanying spike potentials and associated transient increases in [Ca2+]i (Ca2+-transients). Nifedipine abolished the spike potentials but not the slow potentials, and reduced the amplitude of associated Ca2+-transients. Caffeine, in the absence or presence of ryanodine, reduced resting [Ca2+]i levels and abolished the slow potentials and associated Ca2+-transients. Depolarization elevated and hyperpolarization reduced resting [Ca2+]i levels with associated changes in the frequency of slow potentials. The amplitude of Ca2+-transients changed in a bell-shaped manner with the membrane potential change. Slow potentials and associated Ca2+-transients were abolished if [Ca2+]i levels were reduced by BAPTA-AM or if the internal Ca2+ pump was inhibited by cyclopiazonic acid. 2-Aminoethoxy-diphenylborate (2-APB), a known inhibitor of inositol trisphosphate (IP3)-mediated Ca2+ release, also blocked slow potentials and Ca2+-transients. Carbonyl cyanide m-chlorophenyl hydrazone (CCCP), a mitochondrial protonophore, depolarized the membrane, elevated [Ca2+]i levels and abolished slow potentials and Ca2+-transients. Inhibition of mitochondrial ATP-sensitive K+ channels by glybenclamide and 5-hydroxydecanoic acid (5-HAD) abolished slow potentials and Ca2+-transients, without altering the smooth muscle [Ca2+]i. It is concluded that in antrum circular muscles, the frequency of slow potentials is correlated with the level of [Ca2+]i. The slow potential is coupled to release of Ca2+ from an internal store, possibly through the activation of IP3 receptors; this may be initiated by the activation of ATP-sensitive K+ channels in mitochondria following Ca2+ handling by mitochondria.
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