Urinary bladder-urethral sphincter dysfunction in mice with targeted disruption of neuronal nitric oxide synthase models idiopathic voiding disorders in humans

Arthur L. Burnett, David C. Calvin, Shelly L. Chamness, Jian Xiang Liu, Randy J. Nelson, Sabra L. Klein, Valina L. Dawson, Ted M. Dawson, Solonion H. Snyder

Research output: Contribution to journalArticle

Abstract

Idiopathic voiding disorders affect up to 10-15% of men and women. We describe bladder abnormalities in mice with targeted deletion of the gene for neuronal nitric oxide synthase which model the clinical disorders. The mice possess hypertrophic dilated bladders and dysfunctional urinary outlets which do not relax in response to electrical field stimulation or L-arginine. The mice also display increased urinary frequency.

Original languageEnglish (US)
Pages (from-to)571-574
Number of pages4
JournalNature medicine
Volume3
Issue number5
DOIs
StatePublished - Jan 1 1997

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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