Document Detail


The TRPv1 receptor is a mediator of the exercise pressor reflex in rats.
MedLine Citation:
PMID:  20142275     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The skeletal muscle exercise pressor reflex (EPR) induces increases in heart rate (HR) and mean arterial pressure (MAP) during physical activity. This reflex is activated during contraction by stimulation of afferent fibres responsive to mechanical distortion and/or the metabolic by-products of skeletal muscle work. The molecular mechanisms responsible for activating these afferent neurons have yet to be identified. It has been reported that activation of the transient receptor potential vanilloid 1 (TRPv1) receptor within skeletal muscle (localized to unmyelinated afferent fibres) elicits increases in MAP and HR similar to those generated by the EPR. Thus, we hypothesized that stimulation of the TRPv1 receptor during muscle contraction contributes to the activation of the EPR. The EPR was activated by electrically induced static muscle contraction of the hindlimb in decerebrate Sprague-Dawley rats (n = 61) before and after the administration of the TRPv1 receptor antagonists, capsazepine (Capz; 100 microg/100 microl), iodoresinaferatoxin (IRTX; 1 microg/100 microl), or Ruthenium Red (RR; 100 microg/100 microl). Static muscle contraction alone induced increases in both HR (8 +/- 2 bpm) and MAP (21 +/- 3 mmHg). The HR and MAP responses to contraction were significantly lower (P < 0.05) after the administration of Capz (2 +/- 1 bpm; 7 +/- 1 mmHg, respectively), IRTX (3 +/- 2 bpm; 5 +/- 3 mmHg, respectively) and RR (0 +/- 1, bpm; 5 +/- 2 mmHg, respectively). These data suggest that the TRPv1 receptor contributes importantly to activation of the EPR during skeletal muscle contraction in the rat.
Authors:
Scott A Smith; Anna K Leal; Maurice A Williams; Megan N Murphy; Jere H Mitchell; Mary G Garry
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-02-08
Journal Detail:
Title:  The Journal of physiology     Volume:  588     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-04-02     Completed Date:  2010-06-28     Revised Date:  2011-07-27    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1179-89     Citation Subset:  IM    
Affiliation:
Department of Physical Therapy, University of Texas Southwestern Medical Center, Dallas, TX, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects,  physiology
Capsaicin / analogs & derivatives,  pharmacology
Diterpenes / pharmacology
Heart Rate / drug effects,  physiology
Hindlimb / drug effects,  physiopathology
Male
Muscle Contraction / drug effects,  physiology*
Muscle, Skeletal / drug effects,  physiology
Physical Conditioning, Animal / physiology*
Rats
Rats, Sprague-Dawley
Reflex / drug effects,  physiology*
Ruthenium Red / pharmacology
TRPV Cation Channels / antagonists & inhibitors,  drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
HL-070242/HL/NHLBI NIH HHS; HL-088422/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Diterpenes; 0/TRPV Cation Channels; 0/Trpv1 protein, rat; 0/capsazepine; 11103-72-3/Ruthenium Red; 404-86-4/Capsaicin; 57444-62-9/resiniferatoxin
Comments/Corrections

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


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