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  • Title: Beta3-adrenoceptors in urinary bladder.
    Author: Yamaguchi O, Chapple CR.
    Journal: Neurourol Urodyn; 2007; 26(6):752-6. PubMed ID: 17600372.
    Abstract:
    The beta-adrenoceptor (AR) is currently classified into beta(1), beta(2), and beta(3) subtypes. A third subtype, beta(3)-AR, was first identified in adipose tissue, but has also been identified in smooth muscle tissue, particularly in the gastrointestinal tract and urinary bladder smooth muscle. There is a predominant expression of beta(3)-AR messenger RNA (mRNA) in human bladder, with 97% of total beta-AR mRNA being represented by the beta(3)-AR subtype and only 1.5 and 1.4% by the beta(1)-AR and beta (2)-AR subtypes, respectively. Moreover, the presence of beta(1)-, beta(2)-, and beta(3)-AR mRNAs in the urothelium of human bladder has been identified. The distribution of beta-AR subtypes mediating detrusor muscle relaxation is species dependent, the predominant subtype being the beta(3)-AR in humans. Recent studies have suggested that cAMP-dependent routes are not exclusive mechanisms triggering the beta-AR-mediated relaxation of smooth muscle. It has been demonstrated in rats detrusor muscle that cAMP plays a greater role in beta-adrenergic relaxation against basal tone than against KCl-induced tone and that conversely calcium-activated K(+) channels (BKca channels) play a greater role under the latter circumstances. In rat models, beta(3)-AR agonists increase bladder capacity without influencing bladder contraction and have only weak cardiovascular side effects. Although this evidence points toward the clinical utility of beta(3)-AR agonists as therapy for overactive bladder (OAB), pharmacological differences exist between rat and human beta(3)-ARs. Development of compounds with high selectivity for the human beta(3)-AR, identified by screening techniques using cell lines transfected with the human beta(1)-, beta(2)-, and beta(3)-AR genes, may mitigate against such problems. The association between the tryptophan 64 arginine polymorphism in the beta(3)-AR gene and idiopathic OAB is discussed.
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