Abstract
The electrophysiological properties of smooth muscle in the murine lower oesophageal sphincter (LOS) were investigated by intracellular microelectrode recording. Inhibitory junction potentials (IJPs) evoked by trains of field stimulation (30 V, 0.2-0.3 ms, 10 stimuli at 1-50 Hz) were observed in the murine LOS in the presence of atropine (1 μM) and nifedipine (1 μM). The IJP consists of two components, which we termed fast IJP and slow IJP. The fast IJP was partly sensitive to guanethidine (5 μM), pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 30 μM) and apamin (0.1 μM), suggesting that the fast IJP was produced partly through the activation of apamin-sensitive Ca2+-activated K+ channels and of P2-purinoceptors. The other part of the fast IJP was sensitive to Nω-nitro-l-arginine (l-NNA, 100 μM) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one (ODQ, 1 μM), but insensitive to apamin (0.1 μM), iberiotoxin (50 nM) and charybdotoxin (30 nM). Slow IJP was sensitive to l-NNA (100 μM), ODQ (10 μM) and glibenclamide (10 μM), but insensitive to apamin (0.1 μM), iberiotoxin (50 nM) and charybdotoxin (30 nM). KT5823, a protein kinase G (PKG) inhibitor, had no effect on the fast and slow IJP in this tissue. It was suggested that, in the mouse LOS, adenosine trisphosphate (ATP) partly mediated the fast IJP through apamin-sensitive Ca2+-activated K+ channels, and nitric oxide mediated the remained part of the fast IJP and the slow IJP through cGMP, but not PKG. ATP-sensitive K+ channels were suggested to be partly involved in the production of slow IJP, but the responsible channel(s) for the nitrergic fast IJP remained unclarified.
