Abstract:
:The neuronal isoform of nitric oxide synthase (nNOS) is highly expressed in mammalian skeletal muscle, but its functional role has not been defined. NO has been implicated in the local metabolic regulation of blood flow in contracting skeletal muscle in part by antagonizing sympathetic vasoconstriction. We therefore hypothesized that nNOS in skeletal muscle is the source of the NO mediating the inhibition of sympathetic vasoconstriction in contracting muscle. In the mdx mouse, a model of Duchenne muscular dystrophy in which dystrophin deficiency results in greatly reduced expression of nNOS in skeletal muscle, we found that the normal ability of skeletal muscle contraction to attenuate alpha-adrenergic vasoconstriction is defective. Similar results were obtained in mutant mice that lack the gene encoding nNOS. Together these data suggest a specific role for nNOS in the local metabolic inhibition of alpha-adrenergic vasoconstriction in active skeletal muscle.
journal_name
Proc Natl Acad Sci U S Aauthors
Thomas GD,Sander M,Lau KS,Huang PL,Stull JT,Victor RGdoi
10.1073/pnas.95.25.15090subject
Has Abstractpub_date
1998-12-08 00:00:00pages
15090-5issue
25eissn
0027-8424issn
1091-6490journal_volume
95pub_type
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