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Kim HS, Park WJ, Park EY, et al. Role of Nicotinic Acetylcholine Receptor α3 and α7 Subunits in Detrusor Overactivity Induced by Partial Bladder Outlet Obstruction in Rats. Int Neurourol J. 2015;19(1):12-8doi: 10.5213/inj.2015.19.1.12.
Kim, H. S., Park, W. J., Park, E. Y., Koh, J. S., Hwang, T. K., & Kim, J. C. (2015). Role of Nicotinic Acetylcholine Receptor α3 and α7 Subunits in Detrusor Overactivity Induced by Partial Bladder Outlet Obstruction in Rats. International neurourology journal, 19(1), 12-8. https://doi.org/10.5213/inj.2015.19.1.12
Kim, Hyo Sin, et al. "Role of Nicotinic Acetylcholine Receptor α3 and α7 Subunits in Detrusor Overactivity Induced by Partial Bladder Outlet Obstruction in Rats." International neurourology journal vol. 19,1 (2015): 12-8. doi: https://doi.org/10.5213/inj.2015.19.1.12
Kim HS, Park WJ, Park EY, Koh JS, Hwang TK, Kim JC. Role of Nicotinic Acetylcholine Receptor α3 and α7 Subunits in Detrusor Overactivity Induced by Partial Bladder Outlet Obstruction in Rats. Int Neurourol J. 2015 Mar;19(1):12-8. doi: 10.5213/inj.2015.19.1.12. Epub 2015 Mar 26. PMID: 25833476; PMCID: PMC4386486.
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Int Neurourol J. 2015 Mar;19(1):12-8. doi: 10.5213/inj.2015.19.1.12. Epub 2015 Mar 26.

Role of Nicotinic Acetylcholine Receptor α3 and α7 Subunits in Detrusor Overactivity Induced by Partial Bladder Outlet Obstruction in Rats.

International neurourology journal

Hyo Sin Kim, Wang Jin Park, Eun Young Park, Jun Sung Koh, Tae-Kon Hwang, Joon Chul Kim

Affiliations

  1. Department of Urology, The Catholic University of Korea College of Medicine, Seoul, Korea.

PMID: 25833476 PMCID: PMC4386486 DOI: 10.5213/inj.2015.19.1.12

Abstract

PURPOSE: To investigate the role of α3 and α7 nicotinic acetylcholine receptor subunits (nAChRs) in the bladder, using a rat model with detrusor overactivity induced by partial bladder outlet obstruction (BOO).

METHODS: Forty Sprague-Dawley rats were used: 10 were sham-operated (control group) and 30 were observed for 3 weeks after partial BOO. BOO-induced rats were further divided into 3 groups: Two groups of 10 rats each received intravesicular infusions with hexamethonium (HM group; n=10) or methyllycaconitine (MLC group; n=10), which are antagonists for α3 and α7 nAChRs, respectively. The remaining BOO-induced rats received only saline infusion (BOO group; n=10). Based on the contraction interval measurements using cystometrogram, the contraction pressure and nonvoiding bladder contractions were compared between the control and the three BOO-induced groups. Immunofluorescent staining and Western blotting were used to analyze α3 and α7 nAChRs levels.

RESULTS: The contraction interval of the MLC group was higher than that of the BOO group (P<0.05). Nonvoiding bladder contraction almost disappeared in the HM and MLC groups. Contraction pressure increased in the BOO group (P<0.05) compared with the control group and decreased in the HM and MLC groups compared with the BOO group (P<0.05). Immunofluorescence staining showed that the α3 nAChR signals increased in the urothelium, and the α7 nAChR signals increased in the urothelium and detrusor muscle of the BOO group compared with the control group. Western blot analysis showed that both α3 and α7 nAChR levels increased in the BOO group (P<0.05).

CONCLUSIONS: Alpha3 and α7 nAChRs are associated with detrusor overactivity induced by BOO. Furthermore, nAChR antagonists could help in clinically improving detrusor overactivity.

Keywords: Alpha7 Nicotinic Acetylcholine Receptor; Urinary Bladder Neck Obstruction; Urinary Bladder, Overactive

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