Effect of ACE Inhibitor on Connexin Expression after Bladder Outlet Obstruction in Rats.
- Author:
Hyo Sin KIM
1
;
Joon Chul KIM
;
Tae Kon HWANG
Author Information
1. Department of Urology, College of Medicine, The Catholic University of Korea, Seoul, Korea. kjc@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Overactive bladder;
Connexins;
ACE inhibitors
- MeSH:
Angiotensin-Converting Enzyme Inhibitors;
Animals;
Connexin 43;
Connexins;
Models, Animal;
Mucous Membrane;
Peptidyl-Dipeptidase A;
Rats*;
Rats, Sprague-Dawley;
Urinary Bladder Neck Obstruction*;
Urinary Bladder*;
Urinary Bladder, Overactive
- From:Korean Journal of Urology
2005;46(11):1205-1212
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Clinically, bladder outlet obstruction (BOO) causes not only obstructive symptoms but also overactive bladder symptoms which partially result from the increase of electrical coupling in the bladder. This study was performed to determine the effect of angiotensin converting enzyme (ACE) inhibitor on connexin (Cx) expression in overactive bladder caused by BOO in a rat model. MATERIALS AND METHODS: Fifty Sprague-Dawley rats were used for this study and divided into control (10 rats) and experimental (40 rats) groups. Partial obstruction was induced in the experimental group which was divided into two subgroups of 20 rats each: one group administered with ACE inhibitor (ACE inhibitor treated group) and the other without administration (obstruction group). Cystometrograms (CMG) were performed 2 weeks after BOO. The bladders of each group were dissected out and underwent staining for Cx26 and Cx43. RESULTS: On CMG, there was a significant decrease in contraction interval of the obstructive group compared with the control group. The ACE inhibitor treated group showed an increase in contraction interval compared with the obstruction group but a decrease in contraction interval compared with the control group (p<0.05). On immunohistochemical staining, Cx26 was localized in the mucosa and Cx43 in the mucosa and muscle layer. The staining intensity of Cx26 and Cx43 was increased in the obstructive group compared with the control group, but decreased in the ACE inhibitor treated group compared with the obstruction group. CONCLUSIONS: ACE inhibitor decreased the expression of Cx and relieved the overactive bladder symptom. Therefore, ACE inhibitor could be used as alternative agent for the treatment of overactive bladder associated with BOO.