Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat.

Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Research Abstract Details 

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Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Abstract Text:

Hitoshi Masuda,Jang H Kim,Kazunori Kihara,Michael B Chancellor,William C de Groat,Naoki Yoshimura,

OBJECTIVES: To investigate the peripheral role of nitric oxide (NO) in capsaicin-induced detrusor overactivity (DO), as exogenously applied vanilloids can evoke NO release in urothelial cells but its functional role has not yet been reported. MATERIALS AND METHODS: The effects of N(G)-nitro-l-arginine methyl ester (L-NAME), an inhibitor of NO synthase (NOS), on bladder activity during intravesical capsaicin (30 microm) instillation were examined by using continuous infusion cystometry in urethane-anaesthetized rats. L-NAME was administered intravenously (i.v., 20 mg/kg), intrathecally (i.t., 270 microg/rat), intracerebroventricularly (i.c.v., 270 microg/rat) or intravesically (10 mg/mL) before or during capsaicin instillation. RESULTS: During cystometry with intravesical saline infusion, L-NAME injected i.v., i.t. and i.c.v., but not intravesically, significantly increased the intercontraction intervals (ICI) and L-NAME injected i.v., but not i.t., i.c.v. or intravesically, increased the maximum voiding pressure (MVP) without affecting the baseline pressure. Capsaicin instillation induced DO evidenced by a significant reduction in the ICI. L-NAME administered i.v. further decreased the ICI and increased the MVP and the baseline pressure during capsaicin instillation. Co-intravesical application of capsaicin and L-NAME also similarly enhanced capsaicin-induced DO. However, L-NAME injected i.t. or i.c.v. had no effect on capsaicin-induced DO. The excitatory effects of i.v and intravesical L-NAME on the ICI, MVP and baseline pressure during capsaicin infusion were significantly suppressed by desensitization of C-fibre afferent pathways by capsaicin pretreatment (125 mg/kg s.c., 4 days before cystometry). CONCLUSION: These results indicate that locally released NO can suppress DO induced by capsaicin-mediated C-fibre activation and that central NO pathways are not involved in capsaicin-induced DO.

Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Publishing Authors By Initials

H Masuda,JH Kim,K Kihara,MB Chancellor,WC de Groat,N Yoshimura,

For similar tissues: epithelium: urothelium research abstracts see: tissues: epithelium: urothelium research

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Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: BJU international

VOLUME: 100

Page Numbers: 912-8

Journal Abbreviation: BJU Int.

ISSN: 1464-4096

DAY: 27

MONTH: Oct

YEAR: 2007

Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100886721

Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Keywords Mesh Terms:

KEYWORDS: Urothelium

MESH TERMS: physiopathology

Chemical & Substance for Abstract: Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat. Information

Substance Name: Nitric Oxide Synthase

Registry Number: EC 1.14.13.39

Grant and Affiliation Information for Inhibitory roles of peripheral nitrergic mechanisms in capsaicin-induced detrusor overactivity in the rat.

AFFILIATION: Department of Urology and Reproductive Medicine, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan. hi-masu.uro@tmd.ac.jp

Country: England

AGENCY: United States NICHD

GRANT: P01 HD39768

ACRONYM: HD

MEDLINETA: BJU Int

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