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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Arginine / pharmacology
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Disease Models, Animal*
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Electric Stimulation
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Endothelium, Vascular / chemistry
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Humans
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Hypertrophy
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Male
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Mice
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Mice, Inbred C57BL
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Muscle Contraction / drug effects
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Neurons / enzymology
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Nitric Oxide / physiology
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Nitric Oxide Synthase / analysis
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Nitric Oxide Synthase / genetics
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Nitric Oxide Synthase / physiology*
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Nitroprusside / pharmacology
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Urethra / chemistry
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Urethra / physiopathology*
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Urinary Bladder / chemistry
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Urinary Bladder / innervation
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Urinary Bladder / physiopathology*
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Urination Disorders / physiopathology*
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Urothelium / chemistry
Substances
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Nitroprusside
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Nitric Oxide
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Arginine
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Nitric Oxide Synthase