Pharmacological characterization of beta-adrenoceptors mediating relaxation of the rat urinary bladder in vitro.

1. Isoproterenol relaxed KCl-precontracted rat bladder strips with a pD2 of 7.21 leaving a residual contractile response of 3.2% after 30 microM. The selective beta1-agonist, T-0509 (pD2 : 6.24, 10.1% residual contraction after 100 microM), beta2-agonist, terbutaline (pD2 : 5.43, 13.7% residual contraction after 100 microM), and beta3-agonists, BRL 37344A (pD2 : 6.60, 17.3% residual contraction after 100 microM), and SR 58611A (pD2 : 5.15, 34.0% residual contraction after 100 microM), also relaxed bladder strips. 2. The relaxant response to isoproterenol was weakly but significantly antagonized by 1 microM propranolol which produced a 3 fold shift of the concentration-response curve to the right, and significantly antagonized by the beta1-selective antagonist, metoprolol (10 microM, 3 fold shift), and the beta2-selective antagonist, butoxamine (100 microM, 6 fold shift). A combination of 10 microM metoprolol and 100 microM butoxamine caused a 15 fold shift of the concentration-response curve for isoproterenol to the right. Incubation with the beta3-antagonist, SR 59230A (1 microM), caused a 6 fold shift of the concentration response curve for isoproterenol to the right. 3. The non-conventional partial agonist, CGP 12177A, weakly relaxed KCl-precontracted bladder strips (pD2 : 3.31, 51.3% residual contraction after 300 microM); the relaxation was resistant to blockade by 1 or 10 microM propranolol. 4. In the presence of 200 microM propranolol, CGP 12177A (20 microM) or SR 59230A (10 microM) antagonized surmountably the relaxant effects of BRL 37344A. 5. The data suggest that rat urinary bladder body contains beta1, beta2, and beta3-adrenoceptors, all of which mediate relaxation.