Chloride-mediated inhibitory junction potentials in opossum esophageal circular smooth muscle.

Intracellular recordings were made from circular smooth muscle cells of the opossum esophagus. Inhibitory junction potentials (IJPs) 8.3 +/- 0.7 mV in amplitude were observed in response to a single pulse (1 ms, 15 mA) of transmural nerve stimulation. Potassium channel blockers apamin (1 microM), tetraethylammonium (10 mM), 4-aminopyridine (250 microM), and cesium chloride (10 mM) did not reduce IJP amplitude. Conditioning hyperpolarizations to the equilibrium potential for potassium were associated with a significant increase in IJP amplitude. A small increase in membrane resistance was observed during the IJP. Changes in external potassium concentration had no significant effect on IJP amplitude acutely. However, prolonged perfusion with potassium-free Krebs solution resulted in a marked decrease in IJP amplitude as did prolonged perfusion with ouabain (0.1 mM). Low-chloride solution (12.4 mM) resulted acutely in an increase in IJP amplitude. Prolonged low-chloride perfusion resulted in a significant decrease in IJP amplitude. The anion exchange chloride channel inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (600 microM) significantly reduced IJP amplitude. These findings suggest that the IJP observed in opossum esophageal circular smooth muscle in response to a single pulse of stimulation is due to a decrease in membrane chloride conductance. The ability of prolonged application of Na-K pump inhibitors to abolish the IJP appears to be due to known secondary effects of these agents in depleting intracellular chloride.