Electrical components contributing to the nerve-mediated contractions in the smooth muscles of the rabbit ear artery.

Adrenergic transmissions were investigated by recording electrical and mechanical responses of the smooth muscle cells in the rabbit ear artery. Perivascular nerve stimulation generated an excitatory junction potential (e.j.p.) and a slow depolarization. The latter but not the former was suppressed by prazosin or phentolamine. Both the e.j.p. and slow depolarization were suppressed by tetrodotoxin (TTX) or guanethidine. Facilitation processes of e.j.p.s produced by repetitive stimulation of the nerves were not modified by prazosin, phentolamine, or yohimbine. Increasing the stimulus frequency increased the amplitude of e.j.p.s and slow depolarizations and, at high frequencies (greater than 5 Hz) generated a spike potential. Nicardipine (10(-7) M) blocked the spike potential and reduced the e.j.p. amplitude, but did not affect the slow depolarization. Amplitude of muscle contractions produced by transmural nerve stimulation increased with increase in the stimulus frequency. The nerve-mediated contractions produced by high-frequency stimulation (10 Hz) were reduced to 49% of the control value by prazosin (10(-6) M), to 79% by nicardipine (10(-7) M), to 34% by prazosin (10(-6) M) plus nicardipine (10(-7) M), and to 1.2% by TTX (3 X 10(-7) M). Exogenously applied noradrenaline depolarized the smooth muscle membrane and produced the muscle contraction. These effects of noradrenaline were antagonized by prazosin or phentolamine. Thus, in the rabbit ear artery, perivascular nerve stimulation produced three types of electrical responses, i.e., e.j.p., spike potential, and slow depolarization. The latter but not the former two was produced through activation of alpha 1-adrenoceptors. Nerve-mediated muscle contractions were the results of stimulation of alpha 1-adrenoceptors, generation of spike potentials, and of e.j.p.s.