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

Open Access
Publisher Website
Google Scholar
Abstract
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.