Muscarinic receptors mediate cold stress‐induced detrusor overactivity in type 2 diabetes mellitus rats. (8th May 2014)

• Record Type: Journal Article
• Authors: Imamura, Tetsuya; Ishizuka, Osamu; Ogawa, Teruyuki; Yamagishi, Takahiro; Yokoyama, Hitoshi; Minagawa, Tomonori; Nakazawa, Masaki; Gautam, Sudha Silwal; Nishizawa, Osamu
• Is Part Of: International journal of urology. Volume 21:Number 10(2014)
• Page Start: 1051
• Page End: 1058
• Publication Date: 2014-05-08
• Subjects: Urology -- Periodicals; Genitourinary organs -- Periodicals; Urologic Diseases -- Periodicals; 616.6005
• DOI: 10.1111/iju.12475
• Languages: English
• ISSNs: 0919-8172

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="iju12475-sec-0001" sec-type="section"> <title>Objectives</title> <p>This study determined if muscarinic receptors could mediate the cold stress‐induced detrusor overactivity induced in type 2 diabetes mellitus rats.</p> </sec> <sec id="iju12475-sec-0002" sec-type="section"> <title>Methods</title> <p>Ten‐week‐old female Goto‐Kakizaki diabetic rats (<italic>n</italic> = 12) and Wister Kyoto non‐diabetic rats (<italic>n</italic> = 12) were maintained on a high‐fat diet for 4 weeks. Cystometric investigations of the unanesthetized rats were carried out at room temperature (27 ± 2°C) for 20 min. They were intravenously administered imidafenacin (0.3 mg/kg, <italic>n</italic> = 6) or vehicle (<italic>n</italic> = 6). After 5 min, the rats were transferred to a low temperature (4 ± 2°C) for 40 min where the cystometry was continued. The rats were then returned to room temperature for the final cystometric measurements. Afterwards, expressions of bladder muscarinic receptor M<sub>3</sub> and M<sub>2</sub> messenger ribonucleic acids and proteins were assessed by reverse transcription polymerase chain reaction and immunohistochemistry.</p> </sec> <sec id="iju12475-sec-0003" sec-type="section"> <title>Results</title> <p>In non‐diabetic Wister Kyoto rats, imidafenacin did not reduce cold stress‐induced detrusor overactivity. In diabetic Goto‐Kakizaki rats, just after transfer to a low temperature, the cold stress‐induced detrusor overactivity in imidafenacin‐treated rats was reduced compared with vehicle‐treated rats. Within the urinary bladders, the ratio of M<sub>3</sub> to M<sub>2</sub> receptor messenger ribonucleic acid in the diabetic Goto‐Kakizaki rats was significantly higher than that of the non‐diabetic Wister Kyoto rats. The proportion of muscarinic M<sub>3</sub> receptor‐positive area within the detrusor in diabetic Goto‐Kakizaki rats was also significantly higher than that in non‐diabetic Wister Kyoto rats.</p> </sec> <sec id="iju12475-sec-0004" sec-type="section"> <title>Conclusions</title> <p>Imidafenacin partially inhibits cold stress‐induced detrusor overactivity in diabetic Goto‐Kakizaki rats. In this animal model, muscarinic M<sub>3</sub> receptors partially mediate cold stress‐induced detrusor overactivity.</p> </sec> </abstract>