Electrical slow waves in gastrointestinal (GI) muscles are generated by interstitial cells of Cajal (ICC), and these events actively propagate through networks of ICC within the walls of GI organs. The mechanism by which spontaneously active pacemaker sites throughout ICC networks are entrained to produce orderly propagation of slow waves is unresolved. A three-chambered partition bath was used to test the effects of agents that affect metabolism, membrane potential and voltage-dependent Ca(2+) entry on slow wave propagation in canine antral smooth muscle strips. Slow waves evoked by electrical field stimulation actively propagated from end to end of antral muscle strips with a constant latency between two points of recording. When the central chamber of the bath was perfused with low-temperature solutions, mitochondrial inhibitors, reduced extracellular Ca(2+) or blockers of voltage-dependent Ca(2+) channels, active propagation failed. Depolarization or hyperpolarization of the tissue within the central chamber also blocked propagation. Blockade of propagation by reduced extracellular Ca(2+) and inhibitors of dihydropyridine-resistant Ca(2+) channels suggests that voltage-dependent Ca(2+) entry may be the 'entrainment factor' that facilitates active propagation of slow waves in the gastric antrum.
