HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/2/R662    most recent 00214.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Baccari, M. C. Articles by Bani, D. Search for Related Content PubMed PubMed Citation Articles by Baccari, M. C. Articles by Bani, D.

GENETICALLY MODIFIED ANIMALS AND MODEL ORGANISMS

Reversal by relaxin of altered ileal spontaneous contractions in dystrophic (mdx) mice through a nitric oxide-mediated mechanism

Departments of ¹Physiological Sciences and ²Anatomy, Histology and Forensic Medicine, University of Florence, Florence, Italy

Submitted 28 March 2007 ; accepted in final form 23 May 2007

Altered nitric oxide (NO) production/release is involved in gastrointestinal motor disorders occurring in dystrophic (mdx) mice. Since the hormone relaxin (RLX) can upregulate NO biosynthesis, its effects on spontaneous motility and NO synthase (NOS) expression in the ileum of dystrophic (mdx) mice were investigated. Mechanical responses of ileal preparations were recorded in vitro via force-displacement transducers. Evaluation of the expression of NOS isoforms was performed by immunohistochemistry and Western blot. Normal and mdx mice were distributed into three groups: untreated, RLX pretreated, and vehicle pretreated. Ileal preparations from the untreated animals showed spontaneous muscular contractions whose amplitude was significantly higher in mdx than in normal mice. Addition of RLX, alone or together with L-arginine, to the bath medium depressed the amplitude of the contractions in the mdx mice, thus reestablishing a motility pattern typical of the normal mice. The NOS inhibitor N^G-nitro-L-arginine (L-NNA) or the guanylate cyclase inhibitor ODQ reversed the effects of RLX. In RLX-pretreated mdx mice, the amplitude of spontaneous motility was reduced, thus resembling that of the normal mice, and NOS II expression in the muscle coat was increased in respect to the vehicle-pretreated mdx animals. These results indicate that RLX can reverse the altered ileal motility of mdx mice to a normal pattern, likely by upregulating NOS II expression and NO biosynthesis in the ileal smooth muscle.

L-arginine; nitric oxide synthase; muscular dystrophy; intestinal motility

This article has been cited by other articles:

				I. Mookerjee, T. D. Hewitson, M. L. Halls, R. J. Summers, M. L. Mathai, R. A. D. Bathgate, G. W. Tregear, and C. S. Samuel Relaxin inhibits renal myofibroblast differentiation via RXFP1, the nitric oxide pathway, and Smad2 FASEB J, April 1, 2009; 23(4): 1219 - 1229. [Abstract] [Full Text] [PDF]