Literature DB >> 25351368

An update on the pharmacotherapy for lower urinary tract dysfunction.

Nitya Abraham1, Howard B Goldman.   

Abstract

INTRODUCTION: The lower urinary tract (LUT) stores and evacuates urine. It is controlled by autonomic, somatic and sensory innervation. Pharmacotherapy has been developed to optimize neural control of the LUT in pathologic states. AREAS COVERED: The bladder can be overactive or underactive. For overactive bladder, medications targeting various receptors include i) antimuscarinics, ii) mixed-action drugs, iii) β-adrenergic receptor agonists and iv) other medications. There is no effective pharmacotherapy for underactive bladder, although medications have been used with limited success, including i) muscarinic receptor agonists, ii) anticholinesterase inhibitors and iii) α-adrenergic receptor antagonists. At the level of the outlet, there can be decreased resistance resulting in stress urinary incontinence (SUI) or increased resistance resulting in bladder outflow obstruction (BOO). The classes of medications for SUI include i) α-adrenergic receptor agonists, ii) β-adrenergic receptor agonists and iii) antidepressants. Medications used to treat BOO include i) α-adrenergic receptor antagonists, ii) 5-α reductase inhibitors, iii) benzodiazepines, iv) baclofen and v) PDE inhibitors. EXPERT OPINION: Pharmacotherapy for the LUT must be individualized based on degree of bother, medication side-effect profile, concomitant comorbidities, current medication regimen, and insurance coverage. This review describes current medical therapies for the LUT.

Entities:  

Keywords:  bladder outflow obstruction; iatrogenic obstruction; overactive bladder; pharmacotherapy; stress urinary incontinence; underactive bladder; urgency incontinence

Mesh:

Substances:

Year:  2014        PMID: 25351368     DOI: 10.1517/14656566.2015.977253

Source DB:  PubMed          Journal:  Expert Opin Pharmacother        ISSN: 1465-6566            Impact factor:   3.889


  7 in total

Review 1.  Big-conductance Ca2+-activated K+ channels in physiological and pathophysiological urinary bladder smooth muscle cells.

Authors:  Shankar P Parajuli; Yun-Min Zheng; Robert Levin; Yong-Xiao Wang
Journal:  Channels (Austin)       Date:  2016-04-21       Impact factor: 2.581

2.  Novel Thioxothiazolo[3,4-a]quinazolin-5(4H)-one Derivatives as BKCa Channel Activators for Urinary Incontinence.

Authors:  Eun Jung Bae; Heeji Jo; Seong Soon Kim; Dae-Seop Shin; Jung Yoon Yang; Myung Ae Bae; Pyeonghwa Jeong; Chul-Seung Park; Jin Hee Ahn
Journal:  ACS Med Chem Lett       Date:  2022-06-21       Impact factor: 4.632

Review 3.  Potential role of oxidative stress in the pathogenesis of diabetic bladder dysfunction.

Authors:  Qi-Xiang Song; Yi Sun; Kangli Deng; Jin-Yi Mei; Christopher J Chermansky; Margot S Damaser
Journal:  Nat Rev Urol       Date:  2022-08-16       Impact factor: 16.430

Review 4.  Emerging neural stimulation technologies for bladder dysfunctions.

Authors:  Jee Woong Lee; Daejeong Kim; Sangjin Yoo; Hyungsup Lee; Gu-Haeng Lee; Yoonkey Nam
Journal:  Int Neurourol J       Date:  2015-03-26       Impact factor: 2.835

Review 5.  Clinical implications of underactive bladder.

Authors:  Kwang Jin Ko; Chung Un Lee; Kyu-Sung Lee
Journal:  Investig Clin Urol       Date:  2017-11-22

6.  Combination phosphodiesterase type 4 inhibitor and phosphodiesterase type 5 inhibitor treatment reduces non-voiding contraction in a rat model of overactive bladder.

Authors:  Brian M Balog; Abhilasha Tangada; Pooja Sheth; Qi-Xiang Song; Bruna M Couri; Leah L Porras; Gary G Deng; Margot S Damaser
Journal:  PLoS One       Date:  2019-08-28       Impact factor: 3.240

7.  Postmenopausal overactive bladder.

Authors:  Jacek Tomaszewski
Journal:  Prz Menopauzalny       Date:  2014-12-30
  7 in total

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