Abstract
Membrane responses of smooth muscles of the guinea pig mesenteric vein to noradrenaline [norepinephrine] released from perivascular nerves or applied exogenously were investigated. Exogenously applied noradrenaline depolarized the muscle membrane at concentrations > 10-6 M, and generated slow waves or action potentials. Application of phentolamine but not propranolol suppressed the depolarization. The depolarization induced by exogenous noradrenaline was associated with increase in the membrane resistance. The level of the membrane depolarization was modified by changing [K]o, but not by [Na]o or [Cl]o. Repetitive but not single stimulation of the nerves produced slow depolarization of the membrane. The amplitude of the slow depolarization was dependent on the frequency or number of stimuli within a certain range, but beyond this an increased frequency or an increased number of stimulating pulses produced no further increase in amplitude of the slow depolarization. The slow depolarization induced by nerve stimulation was analyzed in relation to the diffusion of transmitter. The rising phase of the slow depolarization fitted well with the theoretically predicted one, while the falling phase did not. Stimulation of nerves with a high frequency and a large number of pulses produced slow waves or action potentials superimposed on the slow depolarization of the membrane. Membrane responses induced by nerve stimulation did not appear in the presence of TTX [tetrodotoxin] or phentolamine. TEA [tetraethylammonium chloride] enhanced the nerve-induced responses. Myogenic electrical activities insensitive to TTX and phentolamine were recorded from the mesenteric vein. These activities were induced by nerve stimulation only in the fresh tissues, were usually irregular in shape, size and frequency, and lasted for 5-20 min. .alpha.-Adrenergic receptors on the muscle membrane reacted in a similar manner to noradrenaline either released from the nerves or applied exogenously. Noradrenaline depolarized the muscle membrane by the decrease in K conductance of the membrane.