Properties of spontaneous activity in gastric smooth muscle

Suzuki, H; Yamamoto, Y; Hirst, GDS

Abstract

Mammalian gastric smooth muscles generate spontaneous rhythmic contractions which are associated with slow oscillatory potentials (slow waves) and spike potentials. Spike potentials are blocked by organic Ca2+-antagonists, indicating that these result from the activation of L-type Ca2+-channel. However, the cellular mechanisms underlying the generation of slow wave remain unclear. Slow waves are insensitive to Ca2+-antagonists but are blocked by metabolic inhibitors or low temperature. Recently it has been suggested that Interstitial Cells of Cajal (ICC) serve as pacemaker cells and a slow wave reflects the coordinated behavior of both ICC and smooth muscle cells. Small segments of circular smooth muscle isolated from antrum of the guinea-pig stomach generated two types of electrical events; irregular small amplitude (1 to 7 mV) of transient depolarization and larger amplitude (20 to 30 mV) of slow depolarization (regenerative potential). Transient depolarization occurred irregularly and membrane depolarization increased their frequency. Regenerative potentials were generated rhythmically and appeared to result from summed transient depolarizations. Spike potentials, sensitive to nifedipine, were generated on the peaks of regenerative potentials. Depolarization of the membrane evoked regenerative potentials with long latencies (1 to 2 s). These potentials had long partial refractory periods (15 to 20 s). They were inhibited by low concentrations of caffeine, perhaps reflecting either depletion of Ca2+ from SR or inhibition of InsP3 receptors, by buffering Ca2+ to low levels with BAPTA or by depleting Ca2+ from SR with CPA. They persisted in the presence of Ca2+-sensitive Cl-channel blockers, niflumic acid and DIDS or Co2+, a non selective Ca2+-channel blocker. These results suggest that spontaneous activity of gastric smooth muscle results from Ca2+ release from SR, followed by activation of Ca2+-dependent ion channels other than Cl- channels, with the release of Ca2+ from SR being triggered by membrane depolarization.