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The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat

Most diabetic patients experience diabetic mellitus (DM) urinary bladder dysfunction. A number of studies evaluate bladder smooth muscle contraction in DM. In this study, we evaluated the change of bladder smooth muscle contraction between normal rats and DM rats. Furthermore, we used pharmacologica...

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Autores principales: Han, Jong Soo, Kim, Su Jin, Nam, Yoonjin, Lee, Hak Yeong, Kim, Geon Min, Kim, Dong Min, Sohn, Uy Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Applied Pharmacology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6319557/
https://www.ncbi.nlm.nih.gov/pubmed/30419634
http://dx.doi.org/10.4062/biomolther.2018.136
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author Han, Jong Soo
Kim, Su Jin
Nam, Yoonjin
Lee, Hak Yeong
Kim, Geon Min
Kim, Dong Min
Sohn, Uy Dong
author_facet Han, Jong Soo
Kim, Su Jin
Nam, Yoonjin
Lee, Hak Yeong
Kim, Geon Min
Kim, Dong Min
Sohn, Uy Dong
author_sort Han, Jong Soo
collection PubMed
description Most diabetic patients experience diabetic mellitus (DM) urinary bladder dysfunction. A number of studies evaluate bladder smooth muscle contraction in DM. In this study, we evaluated the change of bladder smooth muscle contraction between normal rats and DM rats. Furthermore, we used pharmacological inhibitors to determine the differences in the signaling pathways between normal and DM rats. Rats in the DM group received an intraperitoneal injection of 65 mg/kg streptozotocin and measured blood glucose level after 14 days to confirm DM. Bladder smooth muscle contraction was induced using acetylcholine (ACh, 10(−4) M). The materials such as, atropine (a muscarinic receptor antagonist), U73122 (a phospholipase C inhibitor), DPCPX (an adenosine A(1) receptor antagonist), udenafil (a PDE5 inhibitor), prazosin (an α(1)-receptor antagonist), papaverine (a smooth muscle relaxant), verapamil (a calcium channel blocker), and chelerythrine (a protein kinase C inhibitor) were pre-treated in bladder smooth muscle. We found that the DM rats had lower bladder smooth muscle contractility than normal rats. When prazosin, udenafil, verapamil, and U73122 were pre-treated, there were significant differences between normal and DM rats. Taken together, it was concluded that the change of intracellular Ca(2+) release mediated by PLC/IP3 and PDE5 activity were responsible for decreased bladder smooth muscle contractility in DM rats.
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spelling pubmed-63195572019-01-17 The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat Han, Jong Soo Kim, Su Jin Nam, Yoonjin Lee, Hak Yeong Kim, Geon Min Kim, Dong Min Sohn, Uy Dong Biomol Ther (Seoul) Original Article Most diabetic patients experience diabetic mellitus (DM) urinary bladder dysfunction. A number of studies evaluate bladder smooth muscle contraction in DM. In this study, we evaluated the change of bladder smooth muscle contraction between normal rats and DM rats. Furthermore, we used pharmacological inhibitors to determine the differences in the signaling pathways between normal and DM rats. Rats in the DM group received an intraperitoneal injection of 65 mg/kg streptozotocin and measured blood glucose level after 14 days to confirm DM. Bladder smooth muscle contraction was induced using acetylcholine (ACh, 10(−4) M). The materials such as, atropine (a muscarinic receptor antagonist), U73122 (a phospholipase C inhibitor), DPCPX (an adenosine A(1) receptor antagonist), udenafil (a PDE5 inhibitor), prazosin (an α(1)-receptor antagonist), papaverine (a smooth muscle relaxant), verapamil (a calcium channel blocker), and chelerythrine (a protein kinase C inhibitor) were pre-treated in bladder smooth muscle. We found that the DM rats had lower bladder smooth muscle contractility than normal rats. When prazosin, udenafil, verapamil, and U73122 were pre-treated, there were significant differences between normal and DM rats. Taken together, it was concluded that the change of intracellular Ca(2+) release mediated by PLC/IP3 and PDE5 activity were responsible for decreased bladder smooth muscle contractility in DM rats. The Korean Society of Applied Pharmacology 2019-01 2018-11-12 /pmc/articles/PMC6319557/ /pubmed/30419634 http://dx.doi.org/10.4062/biomolther.2018.136 Text en Copyright ©2019, The Korean Society of Applied Pharmacology http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Han, Jong Soo
Kim, Su Jin
Nam, Yoonjin
Lee, Hak Yeong
Kim, Geon Min
Kim, Dong Min
Sohn, Uy Dong
The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title_full The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title_fullStr The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title_full_unstemmed The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title_short The Inhibitory Mechanism on Acetylcholine-Induced Contraction of Bladder Smooth Muscle in the Streptozotocin-Induced Diabetic Rat
title_sort inhibitory mechanism on acetylcholine-induced contraction of bladder smooth muscle in the streptozotocin-induced diabetic rat
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6319557/
https://www.ncbi.nlm.nih.gov/pubmed/30419634
http://dx.doi.org/10.4062/biomolther.2018.136
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