The neural and non‐neural mechanisms involved in urethral activity in rabbits.

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Abstract
The effects of electrical and chemical stimulation on the mechanical or electrical properties of the circular smooth muscle cells of the bladder neck, and proximal urethra of the male rabbit were investigated by means of micro‐electrode, double‐sucrose‐gap and tension‐recording methods. In the bladder neck, application of short current pulses (50 microseconds) produced an initial excitatory junction potential (e.j.p.) with a superimposed spike, followed by a late depolarization, and these electrical events evoked contraction. The initial e.j.p. was unaffected by guanethidine, phentolamine, methysergide or mepyramine, indicating the initial e.j.p. is not mediated by activation of adrenergic, tryptaminergic or histaminergic receptors. The late depolarization was enhanced by pre‐treatment with neostigmine (10(‐7) M) and abolished by atropine (10(‐6) M). In the proximal urethra, electrical‐field stimulation evoked phasic contraction which was followed by relaxation, associated with initial e.j.p.s, late depolarization and inhibitory junction potentials (i.j.p.s). Guanethidine (10(‐5) M) or phentolamine (10(‐6) M) reduced the size of the initial e.j.p. to 40‐50% of the control value and combined application of guanethidine and atropine further reduced the amplitude of the e.j.p. to 20‐30%. There was a parallel reduction in the mechanical response. The late depolarization was enhanced by neostigmine and abolished by atropine. The i.j.p. and muscle relaxation were not affected by propranolol, phentolamine, guanethidine or atropine. These results indicate that the proximal urethral smooth muscle cells are innervated by adrenergic and cholinergic excitatory, and by non‐cholinergic non‐adrenergic inhibitory nerve fibres. In the prostatic urethra, field stimulations also evoked twitch contractions with or without following phasic contraction and relaxation. The twitch contractions were abolished by d‐tubocurarine (10(‐6) M), suggesting that they arise from striated muscle. Exogenously applied prostaglandin (PG) E1, PGE2 or PGF2 alpha (greater than 10(‐10) M) evoked sustained increase in the muscle tone in the presence or absence of indomethacin, and enhanced the amplitude of muscle relaxation evoked by the field stimulation without affecting the resting membrane potential. Indomethacin (10(‐6)‐10(‐5) M) gradually reduced the muscle tone of the proximal urethra with no change in the resting membrane potential. At the reduced muscle tone, electrical‐field stimulation did not evoke muscle relaxation. Thus, the amplitude of muscle relaxation evoked by field stimulation was dependent on the level of muscle tone of the circular muscle strips.(ABSTRACT TRUNCATED AT 400 WORDS)