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Article
Nature Medicine  3, 571 - 574 (1997)
doi:10.1038/nm0597-571

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

Arthur L. Burnett1, David C. Calvin1, Shelly L. Chamness1, Jian-Xiang Liu1, Randy J. Nelson7, Sabra L. Klein7, Valina L. Dawson2, 3, 6, Ted M. Dawson2, 3 & Solomon H. Snyder3, 4, 5, 8

  1Department of Urology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  2Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  3Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  4Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  5Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  6Department of Physiology, and Psychology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  7Department of College of Arts and Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

  8Correspondence should be addressed to S.H.S.

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.

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Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
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