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Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats

The involuntary dual control systems of the autonomic nervous system (ANS) in the bladder of awake spontaneously hypertensive rats (SHRs) were investigated through simultaneous registrations of intravesical and intraabdominal pressures to observe detrusor overactivity (DO) objectively as a core symp...

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Autores principales: Kim, Khae-Hawn, Jin, Long-Hu, Choo, Gwoan-Youb, Lee, Hun-Jae, Choi, Bo-Hwa, Kwak, Jiyeon, Yoon, Sang-Min, Park, Chang-Shin, Lee, Tack
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344265/
https://www.ncbi.nlm.nih.gov/pubmed/22606029
http://dx.doi.org/10.3390/ijms13045048
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author Kim, Khae-Hawn
Jin, Long-Hu
Choo, Gwoan-Youb
Lee, Hun-Jae
Choi, Bo-Hwa
Kwak, Jiyeon
Yoon, Sang-Min
Park, Chang-Shin
Lee, Tack
author_facet Kim, Khae-Hawn
Jin, Long-Hu
Choo, Gwoan-Youb
Lee, Hun-Jae
Choi, Bo-Hwa
Kwak, Jiyeon
Yoon, Sang-Min
Park, Chang-Shin
Lee, Tack
author_sort Kim, Khae-Hawn
collection PubMed
description The involuntary dual control systems of the autonomic nervous system (ANS) in the bladder of awake spontaneously hypertensive rats (SHRs) were investigated through simultaneous registrations of intravesical and intraabdominal pressures to observe detrusor overactivity (DO) objectively as a core symptom of an overactive bladder. SHRs (n = 6) showed the features of overactive bladder syndrome during urodynamic study, especially DO during the filling phase. After injection of the nonselective sympathetic blocking agent labetalol, DO disappeared in 3 of 6 SHRs (50%). DO frequency decreased from 0.98 ± 0.22 min(−1) to 0.28 ± 0.19 min(−1) (p < 0.01), and DO pressure decreased from 3.82 ± 0.57 cm H(2)O to 1.90 ± 0.86 cm H(2)O (p < 0.05). This suggests that the DO originating from the overactive parasympathetic nervous system is attenuated by the nonselective blocking of the sympathetic nervous system. The detailed mechanism behind this result is still not known, but parasympathetic overactivity seems to require overactive sympathetic nervous system activity in a kind of balance between these two systems. These findings are consistent with recent clinical findings suggesting that patients with idiopathic overactive bladder may have ANS dysfunction, particularly a sympathetic dysfunction. The search for newer and better drugs than the current anticholinergic drugs as the mainstay for overactive bladder will be fueled by our research on these sympathetic mechanisms. Further studies of this principle are required.
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spelling pubmed-33442652012-05-17 Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats Kim, Khae-Hawn Jin, Long-Hu Choo, Gwoan-Youb Lee, Hun-Jae Choi, Bo-Hwa Kwak, Jiyeon Yoon, Sang-Min Park, Chang-Shin Lee, Tack Int J Mol Sci Article The involuntary dual control systems of the autonomic nervous system (ANS) in the bladder of awake spontaneously hypertensive rats (SHRs) were investigated through simultaneous registrations of intravesical and intraabdominal pressures to observe detrusor overactivity (DO) objectively as a core symptom of an overactive bladder. SHRs (n = 6) showed the features of overactive bladder syndrome during urodynamic study, especially DO during the filling phase. After injection of the nonselective sympathetic blocking agent labetalol, DO disappeared in 3 of 6 SHRs (50%). DO frequency decreased from 0.98 ± 0.22 min(−1) to 0.28 ± 0.19 min(−1) (p < 0.01), and DO pressure decreased from 3.82 ± 0.57 cm H(2)O to 1.90 ± 0.86 cm H(2)O (p < 0.05). This suggests that the DO originating from the overactive parasympathetic nervous system is attenuated by the nonselective blocking of the sympathetic nervous system. The detailed mechanism behind this result is still not known, but parasympathetic overactivity seems to require overactive sympathetic nervous system activity in a kind of balance between these two systems. These findings are consistent with recent clinical findings suggesting that patients with idiopathic overactive bladder may have ANS dysfunction, particularly a sympathetic dysfunction. The search for newer and better drugs than the current anticholinergic drugs as the mainstay for overactive bladder will be fueled by our research on these sympathetic mechanisms. Further studies of this principle are required. Molecular Diversity Preservation International (MDPI) 2012-04-23 /pmc/articles/PMC3344265/ /pubmed/22606029 http://dx.doi.org/10.3390/ijms13045048 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Kim, Khae-Hawn
Jin, Long-Hu
Choo, Gwoan-Youb
Lee, Hun-Jae
Choi, Bo-Hwa
Kwak, Jiyeon
Yoon, Sang-Min
Park, Chang-Shin
Lee, Tack
Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title_full Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title_fullStr Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title_full_unstemmed Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title_short Nonselective Blocking of the Sympathetic Nervous System Decreases Detrusor Overactivity in Spontaneously Hypertensive Rats
title_sort nonselective blocking of the sympathetic nervous system decreases detrusor overactivity in spontaneously hypertensive rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3344265/
https://www.ncbi.nlm.nih.gov/pubmed/22606029
http://dx.doi.org/10.3390/ijms13045048
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