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Spontaneous electrical activity and associated changes in calcium concentration in guinea-pig gastric smooth muscle

Hiroyasu Fukuta, Yoshihiko Kito and Hikaru Suzuki

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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