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1 Dipartimento Farmaco-Biologico, Università della Calabria, 87036 Arcavacata di Rende (CS); 2 Dipartimento di Anatomia, Istologia, e Medicina Legale, Università di Firenze, 50134 Florence; and 3 Dipartimento di Biologia cellulare e dello Sviluppo, Università di Palermo, 90128 Palermo, Italy
The aim of the present study
was to evaluate whether alterations in the distribution and/or function
of nitric oxide synthase (NOS) could be involved in the development of
the spontaneous mechanical tone observed in colon from dystrophic
(mdx) mice. By recording the intraluminal pressure of
isolated colon from normal mice, we showed that
N
-nitro- L-arginine methyl
ester (L-NAME) increased the tone, even in the presence of
tetrodotoxin. The effect was prevented by L-arginine, nifedipine, or Ca2+-free solution. In colon from
mdx mice, L-NAME was ineffective. Immunohistochemistry revealed that the presence and distribution of
neuronal (nNOS), endothelial, and inducible NOS isoforms in smooth
muscle cells and neurons of colon from mdx mice were the same as in controls. However, the expression of myogenic nNOS was
markedly reduced in mdx mice. We conclude that there is a myogenic NOS in mouse colon that can tonically produce nitric oxide to
limit influx of Ca2+ through L-type voltage-dependent
channels and modulate the mechanical tone. This mechanism appears to be
defective in mdx mice.
nitric oxide synthase; nitric oxide; Duchenne muscular dystrophy; intestinal smooth muscle; spontaneous tone; immunohistochemistry
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M. C. Baccari, S. Nistri, M. G. Vannucchi, F. Calamai, and D. Bani Reversal by relaxin of altered ileal spontaneous contractions in dystrophic (mdx) mice through a nitric oxide-mediated mechanism Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2007; 293(2): R662 - R668. [Abstract] [Full Text] [PDF] |
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