Cyclic Adenosine Monophosphate Production and Contractile Response Induced by Beta-Adrenoceptor Subtypes in Rabbit Urinary Bladder Smooth Muscle

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Abstract
The spontaneous contractile force of muscle strips isolated from male rabbit urinary bladder dome (detrusor) and base (trigonal muscle) was dose dependently inhibited by isoproterenol, a non-specific beta-adrenoceptor agonist. The relaxant response to 10––6M isoproterenol in the detrusor muscle was completely blocked by butoxamine (10––4M), a selective beta-2-antagonist, and by propranolol (10––6M), a non-specific beta-antagonist, but not by metopronol (10––6 to 10––4M), a selective beta-1-antagonist. Relaxation of trigonal muscle induced by 10––6M isoproterenol was inhibited 30% by metoprolol (10––5M), 70% by butoxamine (10––4M), and 100% by propranolol (10––6M). Terbutaline, a selective beta-2-adrenoceptor agonist, also caused dose dependently a relaxant response in detrusor and trigonal muscle. The maximum relaxant responses to isoproterenol and terbutaline were significantly greater in detrusor than in trigonal muscle. Dobutamine, a relatively specific beta-1-adrenoceptor agonist, caused a small but significant relaxant response in trigonal, but no change in detrusor muscle. In trigonal muscle the relaxant response to dobutamine was less than that to terbutaline. Cyclic adenosine monophosphate accumulation in detrusor did not significantly increase after administration of dobutamine, but significantly increased after administration of terbutaline. On the other hand, not only terbutaline, but also dobutamine, markedly increased cyclic adenosine monophosphate accumulation in trigonal muscle. These findings are consistent with the detrusor having a greater density of beta-adrenoceptors than trigonal muscle and with the relaxant responses to beta-adrenoceptors being mediated by the beta-2-subtype in the detrusor and by both beta-1 – and beta-2-subtypes in trigonal muscle of the rabbit through cyclic adenosine monophosphate accumulation.

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