Neuronal-derived nitric oxide modulates the activity of mouse detrusor smooth muscle

E. Meng, J. S. Young, T. L. Cha, G. H. Sun, D. S. Yu, A. F. Brading

Research output: Contribution to journalArticlepeer-review

Abstract

Aims We investigated the roles of neuronal-derived nitric oxide (NO) in the modulation of spontaneous activity of mouse detrusor smooth muscle. Methods Detrusor smooth muscle strips were isolated from nNOS gene knock-out (nNOS -/-) mice and their wild type siblings (nNOS +/+). The properties of smooth muscle cells were assessed using intracellular electrophysiology and Ca 2+ imaging by laser-scanning confocal microscopy. The effects of an nNOS inhibitor, 7-nitro indazole (7-NI) on electrically evoked contractility were assessed using nNOS +/+ mouse detrusor strips. Results In spontaneously active cells, the frequency of spontaneous action potentials (sAPs) and whole cell Ca 2+ flashes in nNOS -/- preparations was lower than that in the nNOS +/+ preparations. The frequency of sAPs was enhanced by a nitric oxide donor, diethylamine NONOate sodium salt (NONOate; 100μM), both when used alone and when the cGMP pathway was blocked by 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, 10μM). 7-NI (100μM) significantly suppressed the electrically evoked contraction of mouse detrusor strips. Conclusions We suggest that neuronal-derived NO facilitates the generation of spontaneous activity via a cGMP-independent pathway, and consequently enhances the evoked contraction of detrusor. Dysregulation of nNOS containing nerves may underlie bladder pathologies. Copyright © 2012 Wiley Periodicals, Inc.
Original languageEnglish
Pages (from-to)572-578
Number of pages7
JournalNeurourology and Urodynamics
Volume31
Issue number4
Early online date24 Jan 2012
DOIs
Publication statusE-pub ahead of print - 24 Jan 2012
Externally publishedYes

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