Document Detail

Blockade of the sympathetic nervous system degrades ligament in a rat MCL model.
MedLine Citation:
PMID:  14527964     Owner:  NLM     Status:  MEDLINE    
We hypothesize that blockade of the sympathetic nervous system degrades ligament. We tested this hypothesis in a rat medial collateral ligament (MCL) model. Fifteen animals were treated for 10 days with the sympathetic chemotoxin guanethidine using osmotic pumps, whereas 15 control rats received pumps containing saline. A reduction in plasma concentrations of norepinephrine in the guanethidine rats indicated a significant decrease in sympathetic nerve activity. Vasoactive intestinal peptide and neuropeptide Y were decreased in MCLs from guanethidine animals, as quantified by radioimmunoassays. Tissue vascularity was substantially increased in guanethidine MCLs, whereas mechanical properties were significantly decreased. Proteases, such as matrix metalloproteinases (MMP) and cysteine proteases, play a major role in ligament degradation. The proteases MMP-13, cathepsin K, and tartrate-resistant acid phosphatase (TRAP) have collagenolytic activity and have been shown in rat ligament tissues. To determine whether the degradation seen in this study was due to protease activity, we determined the expression of these enzymes in control and treated MCLs. Real-time quantitative PCR revealed that guanethidine treatment increased expression of MMP-13 and cathepsin K mRNAs, although overall expression levels of MMP-13 and TRAP were relatively low. Histology also identified increases in TRAP and cathepsin K, but not MMP-13, in guanethidine-treated tissues. Results support our hypothesis that blockade of the sympathetic nervous system substantially degrades ligament.
Kelley W Dwyer; Paolo P Provenzano; Peter Muir; Wilmot B Valhmu; Ray Vanderby
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2003-10-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  96     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-12     Completed Date:  2004-09-14     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  711-8     Citation Subset:  IM    
Department of Orthopedics and Rehabilitation, University of Wisconsin, Madison, Wisconsin 53792, USA.
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MeSH Terms
Acid Phosphatase / metabolism
Calcitonin Gene-Related Peptide / metabolism
Cathepsin K
Cathepsins / metabolism
Collagenases / metabolism
Guanethidine / pharmacology*
Isoenzymes / metabolism
Matrix Metalloproteinase 1 / metabolism
Matrix Metalloproteinase 13
Medial Collateral Ligament, Knee / innervation*,  physiology*
Neuropeptide Y / metabolism
Norepinephrine / blood
Organ Culture Techniques
Rats, Wistar
Substance P / metabolism
Sympathetic Nervous System / drug effects,  physiology*
Sympatholytics / pharmacology*
Tissue Engineering
Vasoactive Intestinal Peptide / metabolism
Reg. No./Substance:
0/Isoenzymes; 0/Neuropeptide Y; 0/Sympatholytics; 33507-63-0/Substance P; 37221-79-7/Vasoactive Intestinal Peptide; 51-41-2/Norepinephrine; 55-65-2/Guanethidine; 83652-28-2/Calcitonin Gene-Related Peptide; EC 3.1.3.-/tartrate-resistant acid phosphatase; EC Phosphatase; EC 3.4.-/Cathepsins; EC K; EC protein, rat; EC 3.4.24.-/Collagenases; EC 3.4.24.-/Matrix Metalloproteinase 13; EC 3.4.24.-/Mmp13 protein, rat; EC Metalloproteinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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