The contribution of α-adrenoceptors to neurally-mediated contractions of the rabbit urethral smooth muscle

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Abstract
1 The nature of the nerve-mediated contractions in the urethral smooth muscle from the rabbit was studied in vitro. Field stimulation caused smaller contractile responses than in the detrusor of the rabbit. 2 There was no significant difference in response to field stimulation or exogenous agents acting on adrenoceptors between longitudinal and circular strips from the rabbit urethra. Histological studies showed that the urethral muscle is arranged in three layers, which run circularly and longitudinally. 3 Atropine had very little effect on the response to field stimulation, phentolamine almost abolished the contractile response to nerve stimulation and sometimes unmasked a relaxation. 4 The α1-adrenoceptor blocking agent, prazosin, blocked both the contractile response to the α1-receptor agonist phenylephrine and that to intrinsic nerve stimulation, with similar potencies. The α2-blocking agent yohimbine shifted the dose-response curve of the contractile response to the α2-agonist, clonidine, in a dose-dependent manner, 10−7 m causing a 10 fold shift. This concentration had no effect on the response to intrinsic nerve stimulation, suggesting that α2-receptors are not involved in the response. Higher concentrations of yohimbine caused a suppression of the nerve-evoked response which is assumed to be non-specific. 5 Noradrenaline, phenylephrine, and clonidine caused dose-dependent contractile responses in the rabbit urethral strips. The contractions induced by clonidine developed more slowly than those induced by noradrenaline and phenylephrine. 6 These results demonstrate that the rabbit urethral smooth muscle contains both α1- and α2-adrenoceptors, and the nerve-mediated contraction of the rabbit urethra is adrenergic in nature and mediated mainly via α1-adrenoceptors.