Isoproterenol relaxed KCl-precontracted rat bladder strips with a pD2 of 7.21 leaving a residual contractile response of 3.2% after 30 μM. The selective β1-agonist, T-0509 (pD2 : 6.24, 10.1% residual contraction after 100 μM), β2-agonist, terbutaline (pD2 : 5.43, 13.7% residual contraction after 100 μM), and β3-agonists, BRL 37344A (pD2 : 6.60, 17.3% residual contraction after 100 μM), and SR 58611A (pD2 : 5.15, 34.0% residual contraction after 100 μM), also relaxed bladder strips.
The relaxant response to isoproterenol was weakly but significantly antagonized by 1 μM propranolol which produced a 3 fold shift of the concentration-response curve to the right, and significantly antagonized by the β1-selective antagonist, metoprolol (10 μM, 3 fold shift), and the β2-selective antagonist, butoxamine (100 μM, 6 fold shift). A combination of 10 μM metoprolol and 100 μM butoxamine caused a 15 fold shift of the concentration-response curve for isoproterenol to the right. Incubation with the β3-antagonist, SR 59230A (1 μM), caused a 6 fold shift of the concentration response curve for isoproterenol to the right.
The non-conventional partial agonist, CGP 12177A, weakly relaxed KCl-precontracted bladder strips (pD2 : 3.31, 51.3% residual contraction after 300 μM); the relaxation was resistant to blockade by 1 or 10 μM propranolol.
In the presence of 200 μM propranolol, CGP 12177A (20 μM) or SR 59230A (10 μM) antagonized surmountably the relaxant effects of BRL 37344A.
The data suggest that rat urinary bladder body contains β1, β2, and β3-adrenoceptors, all of which mediate relaxation.
British Journal of Pharmacology (1999) 127, 1744–1750; doi:10.1038/sj.bjp.0702709