Augmentation of rat urinary bladder relaxation mediated by β 1-adrenoceptors in experimental diabetes

Abstract

We examined how diabetes affects the β-adrenoceptor subtypes mediating relaxation of rat urinary bladder smooth muscle contracted with carbachol. The relaxant responses to isoproterenol were larger in muscles from rats 8 to 10 weeks after induction of diabetes with streptozotocin (80 mg/kg, i.p.) as compared to the control muscles. In contrast, forskolin-induced relaxations did not differ significantly in the control and diabetes groups. Propranolol (1 μM) abolished the diabetes-induced augmentation of relaxant responses to isoproterenol. The relaxant responses to T-0509 ((−)-( R)-1-(3,4-dihydroxyphenyl)-2-[(3,4-dimethoxyphenethyl)-amino]ethanol hydrochloride), a β 1-adrenoceptor agonist, were small but significantly augmented by diabetes. On the other hand, diabetes did not change the relaxations produced by clenbuterol, a β 2-adrenoceptor agonist, and BRL37344 ((±)-( R*, R*)-(4-[2-([2-(3-chlorophenyl)-2-hydroxyethyl]amino)propyl]phenoxy)acetic acid), a β 3-adrenoceptor agonist. These results suggest that diabetes selectively augments the β 1-adrenoceptor-mediated relaxation of the rat urinary bladder smooth muscle.