Abstract
The membrane potential of dog tracheal muscle was stable at -59.2mV. The length constant of the muscle tissue was 3.2mm and the time constant of the membrane was 449msec. Outward current pulses could not evoke a spike and showed marked rectification of the membrane.Tetraethylammonium, TEA, depolarized the membrane, suppressed the rectification of the membrane, and increased the membrane resistance, and in the presence of TEA outward current pulses could evoke a spike. Acetylcholine and histamine depolarized the membrane but could not evoke a spike. Mechanical response could be evoked by field stimulation via either nerve stimulation or direct muscle stimulation. The mechanical response induced by nerve stimulation was markedly suppressed by atropine. Phentolamine suppressed the contraction which was produced in the presence of atropine, and propranolol suppressed the relaxation. It is unlikely that nonadrenergic-non-cholinergic inhibitory nerves played an important role in the mechanical response. It is concluded regarding the neural actions to the dog trachea that a constriction is induced by cholinergic and adrenergic α-action and a dilation is induced by adrenergic β-action.The relationship between the membrane potential and tension was measured in various [K]O. The mechanical response was triggered by only 5mV depolarization. The physiological evidence and histological finding were compared in relation to nerve activity on the tracheal muscle activity.
