Low-sodium resistant non-adrenergic inhibitory neurotransmission in the guinea-pig duodenum

The evoked inhibitory potentials (i.p.s) in the longitudinal smooth muscle cells of the guinea-pig duodenum were recorded intracellularly. The i.p.s were not blocked by adrenergic blocking agents, guanethidine (10(-6) g/ml), propranolol (10(-6) g/ml) and phentolamine (10(-6) g/ml), and atropine (10(-6) g/ml). Tetrodotoxin (10(-7)-10(-6) g/ml) abolished the non-adrenergic non-cholinergic i.p.s evoked by single or repeated stimulation without changes in the resting membrane potential of the longitudinal smooth muscle. In the presence of atropine (10(-6) g/ml), acetylcholine (5 X 10(-9)-7 X 10(-7) g/ml) had no effect on the amplitude of the i.p.s d-tubocurarine (2 X 10(-5) g/ml) reduced the amplitude of the i.p.s and produced a small depolarization in the muscle membrane. The longitudinal muscle membrane was slightly depolarized by Li-solution and the i.p.s could be evoked in the Li-solution for a long period, accompanying with the slight decrease in the amplitude of the i.p.s. In the choline-solution, the depolarization of the muscle membrane and the slight increase in the amplitude of the i.p.s were obtained. The i.p.s were abolished in the Ca2+-free choline-solution. In the sucrose-solution, the decrease of the resting membrane potential of the longitudinal smooth muscle was observed and the amplitude of the i.p.s was gradually reduced during the perfusion of the sucrose-solution. Chloride deficiency had no considerable effect on the amplitude of i.p.s. The results obtained suggest that the non-adrenergic non-cholinergic inhibitory neurotransmission is low-sodium resistant and the excitation-secretion coupling in the non-adrenergic non-cholinergic inhibitory nerves is mainly dependent on the external calcium ions but not sodium ions.