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Physiological Reviews, Vol. 81, No. 1, January 2001, pp. 209-237
Copyright ©2001 by the American Physiological Society
Howard Hughes Medical Institute, Department of Medicine, Divisions of Pulmonary and Cardiology and Department of Biochemistry, Duke University Medical Center, Durham, North Carolina; and Departments of Biochemistry and Biophysics and of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, North Carolina
Stamler, Jonathan S. and
Gerhard Meissner.
Physiology of Nitric Oxide in Skeletal Muscle. Physiol. Rev. 81: 209-237, 2001.
In the past five years, skeletal muscle has emerged as a
paradigm of "nitric oxide" (NO) function and redox-related
signaling in biology. All major nitric oxide synthase (NOS) isoforms,
including a muscle-specific splice variant of neuronal-type (n)
NOS, are expressed in skeletal muscles of all mammals. Expression and
localization of NOS isoforms are dependent on age and developmental
stage, innervation and activity, history of exposure to cytokines and growth factors, and muscle fiber type and species. nNOS in particular may show a fast-twitch muscle predominance. Muscle NOS localization and activity are regulated by a number of protein-protein
interactions and co- and/or posttranslational modifications.
Subcellular compartmentalization of the NOSs enables distinct functions
that are mediated by increases in cGMP and by
S-nitrosylation of proteins such as the ryanodine receptor-calcium release channel. Skeletal muscle functions
regulated by NO or related molecules include force production
(excitation-contraction coupling), autoregulation of blood flow,
myocyte differentiation, respiration, and glucose homeostasis. These
studies provide new insights into fundamental aspects of muscle
physiology, cell biology, ion channel physiology, calcium homeostasis,
signal transduction, and the biochemistry of redox-related systems.
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R. W. Grange, T. G. Gainer, K. M. Marschner, R. J. Talmadge, and J. T. Stull Fast-twitch skeletal muscles of dystrophic mouse pups are resistant to injury from acute mechanical stress Am J Physiol Cell Physiol, October 1, 2002; 283(4): C1090 - C1101. [Abstract] [Full Text] [PDF]
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Y. Hosaka, T. Yokota, Y. Miyagoe-Suzuki, K. Yuasa, M. Imamura, R. Matsuda, T. Ikemoto, S. Kameya, and S.'i. Takeda {alpha}1-Syntrophin-deficient skeletal muscle exhibits hypertrophy and aberrant formation of neuromuscular junctions during regeneration J. Cell Biol., September 16, 2002; 158(6): 1097 - 1107. [Abstract] [Full Text] [PDF]
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 U. Schara, M. Vorgerd, N. Popovic, B. G.H. Schoser, K. Ricker, and W. Mortier Rippling Muscle Disease in Childhood J Child Neurol, July 1, 2002; 17(7): 483 - 490. [Abstract] [PDF]
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B. Chavoshan, M. Sander, T. E Sybert, J. Hansen, R. G Victor, and G. D Thomas Nitric oxide-dependent modulation of sympathetic neural control of oxygenation in exercising human skeletal muscle J. Physiol., April 1, 2002; 540(1): 377 - 386. [Abstract] [Full Text] [PDF]
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 M. Vorgerd, K. Ricker, F. Ziemssen, W. Kress, H. H. Goebel, W. A. Nix, C. Kubisch, B. G.H. Schoser, and W. Mortier A sporadic case of rippling muscle disease caused by a de novo caveolin-3 mutation Neurology, December 26, 2001; 57(12): 2273 - 2277. [Abstract] [Full Text] [PDF]
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J. Sun, C. Xin, J. P. Eu, J. S. Stamler, and G. Meissner Cysteine-3635 is responsible for skeletal muscle ryanodine receptor modulation by NO PNAS, September 13, 2001; (2001) 201289098. [Abstract] [Full Text] [PDF]
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 C. R. RICHMONDS and H. J. KAMINSKI Nitric oxide synthase expression and effects of nitric oxide modulation on contractility of rat extraocular muscle FASEB J, August 1, 2001; 15(10): 1764 - 1770. [Abstract] [Full Text] [PDF]
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L. W. Smith, J. D. Smith, and D. S. Criswell Involvement of nitric oxide synthase in skeletal muscle adaptation to chronic overload J Appl Physiol, May 1, 2002; 92(5): 2005 - 2011. [Abstract] [Full Text] [PDF]
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J. Sun, L. Xu, J. P. Eu, J. S. Stamler, and G. Meissner Classes of Thiols That Influence the Activity of the Skeletal Muscle Calcium Release Channel J. Biol. Chem., May 4, 2001; 276(19): 15625 - 15630. [Abstract] [Full Text] [PDF]
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G. Zeidner, R. Sadja, and E. Reuveny Redox-dependent Gating of G Protein-coupled Inwardly Rectifying K+ Channels J. Biol. Chem., September 14, 2001; 276(38): 35564 - 35570. [Abstract] [Full Text] [PDF]
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J. Sun, C. Xin, J. P. Eu, J. S. Stamler, and G. Meissner Cysteine-3635 is responsible for skeletal muscle ryanodine receptor modulation by NO PNAS, September 25, 2001; 98(20): 11158 - 11162. [Abstract] [Full Text] [PDF]
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