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      Bladder Dysfunction in Diabetes Mellitus

      review-article
      1 , 1
      Frontiers in Pharmacology
      Frontiers Research Foundation
      diabetes, neurogenic bladder, cystopathy, incontinence

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          Abstract

          Diabetic cystopathy is a well-recognized complication of diabetes mellitus, which usually develops in middle-aged or elderly patients with long-standing and poorly controlled disease. It may have broad spectrum clinical presentations. Patients may be asymptomatic, or have a wide variety of voiding complaints from overactive bladder and urge incontinence to decreased bladder sensation and overflow incontinence. This review focuses on pathophysiological mechanisms responsible for urologic complications of diabetes and emphasizing on recent developments in our understanding of this condition. We also tried to shed some light on therapeutic modalities like behavioral, pharmacological, and surgical approaches.

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          Most cited references85

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          Muscarinic receptors: their distribution and function in body systems, and the implications for treating overactive bladder.

          1. The effectiveness of antimuscarinic agents in the treatment of the overactive bladder (OAB) syndrome is thought to arise through blockade of bladder muscarinic receptors located on detrusor smooth muscle cells, as well as on nondetrusor structures. 2. Muscarinic M3 receptors are primarily responsible for detrusor contraction. Limited evidence exists to suggest that M2 receptors may have a role in mediating indirect contractions and/or inhibition of detrusor relaxation. In addition, there is evidence that muscarinic receptors located in the urothelium/suburothelium and on afferent nerves may contribute to the pathophysiology of OAB. Blockade of these receptors may also contribute to the clinical efficacy of antimuscarinic agents. 3. Although the role of muscarinic receptors in the bladder, other than M3 receptors, remains unclear, their role in other body systems is becoming increasingly well established, with emerging evidence supporting a wide range of diverse functions. Blockade of these functions by muscarinic receptor antagonists can lead to similarly diverse adverse effects associated with antimuscarinic treatment, with the range of effects observed varying according to the different receptor subtypes affected. 4. This review explores the evolving understanding of muscarinic receptor functions throughout the body, with particular focus on the bladder, gastrointestinal tract, eye, heart, brain and salivary glands, and the implications for drugs used to treat OAB. The key factors that might determine the ideal antimuscarinic drug for treatment of OAB are also discussed. Further research is needed to show whether the M3 selective receptor antagonists have any advantage over less selective drugs, in leading to fewer adverse events.
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            Altered urinary bladder function in mice lacking the vanilloid receptor TRPV1.

            In the urinary bladder, the capsaicin-gated ion channel TRPV1 is expressed both within afferent nerve terminals and within the epithelial cells that line the bladder lumen. To determine the significance of this expression pattern, we analyzed bladder function in mice lacking TRPV1. Compared with wild-type littermates, trpv1(-/-) mice had a higher frequency of low-amplitude, non-voiding bladder contractions. This alteration was accompanied by reductions in both spinal cord signaling and reflex voiding during bladder filling (under anesthesia). In vitro, stretch-evoked ATP release and membrane capacitance changes were diminished in bladders excised from trpv1(-/-) mice, as was hypoosmolality-evoked ATP release from cultured trpv1(-/-) urothelial cells. These findings indicate that TRPV1 participates in normal bladder function and is essential for normal mechanically evoked purinergic signaling by the urothelium.
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              Alpha1-, alpha2- and beta-adrenoceptors in the urinary bladder, urethra and prostate.

              1 We have systematically reviewed the presence, functional responses and regulation of alpha(1)-, alpha(2)- and beta-adrenoceptors in the bladder, urethra and prostate, with special emphasis on human tissues and receptor subtypes. 2 Alpha(1)-adrenoceptors are only poorly expressed and play a limited functional role in the detrusor. Alpha(1)-adrenoceptors, particularly their alpha(1A)-subtype, show a more pronounced expression and promote contraction of the bladder neck, urethra and prostate to enhance bladder outlet resistance, particularly in elderly men with enlarged prostates. Alpha(1)-adrenoceptor agonists are important in the treatment of symptoms of benign prostatic hyperplasia, but their beneficial effects may involve receptors within and outside the prostate. 3 Alpha(2)-adrenoceptors, mainly their alpha(2A)-subtype, are expressed in bladder, urethra and prostate. They mediate pre-junctional inhibition of neurotransmitter release and also a weak contractile effect in the urethra of some species, but not humans. Their overall post-junctional function in the lower urinary tract remains largely unclear. 4 Beta-adrenoceptors mediate relaxation of smooth muscle in the bladder, urethra and prostate. The available tools have limited the unequivocal identification of receptor subtypes at the protein and functional levels, but it appears that the beta(3)- and beta(2)-subtypes are important in the human bladder and urethra, respectively. Beta(3)-adrenoceptor agonists are promising drug candidates for the treatment of the overactive bladder. 5 We propose that the overall function of adrenoceptors in the lower urinary tract is to promote urinary continence. Further elucidation of the functional roles of their subtypes will help a better understanding of voiding dysfunction and its treatment.
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                Author and article information

                Journal
                Front Pharmacol
                Front. Pharmacol.
                Frontiers in Pharmacology
                Frontiers Research Foundation
                1663-9812
                29 September 2010
                16 November 2010
                2010
                : 1
                : 136
                Affiliations
                [1] 1simpleDepartment of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia Vancouver, BC, Canada
                Author notes

                Edited by: Eliot Ohlstein, Drexel Med School, USA

                Reviewed by: Eliot Ohlstein, Drexel Med School, USA; Donna Jayne Sellers, Bond University, Australia

                *Correspondence: Ismail Laher, Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada V6T 1Z3.e-mail: ilaher@ 123456interchange.ubc.ca

                This article was submitted to Frontiers in Cardiovascular and Smooth Muscle Pharmacology, a specialty of Frontiers in Pharmacology.

                Article
                10.3389/fphar.2010.00136
                3153010
                21833175
                cd30cdd0-e4d8-4ad3-b978-6aa04623ecd3
                Copyright © 2010 Golbidi and Laher.

                This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

                History
                : 22 September 2010
                : 29 October 2010
                Page count
                Figures: 1, Tables: 0, Equations: 0, References: 97, Pages: 9, Words: 9340
                Categories
                Pharmacology
                Review Article

                Pharmacology & Pharmaceutical medicine
                incontinence,diabetes,neurogenic bladder,cystopathy
                Pharmacology & Pharmaceutical medicine
                incontinence, diabetes, neurogenic bladder, cystopathy

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