The TRPv1 receptor is a mediator of the exercise pressor reflex in rats
Source: The Journal of Physiology, Volume 588, Number 7, April 2010 , pp. 1179-1189(11)
Abstract: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 g/100 l), iodoresinaferatoxin (IRTX; 1 g/100 l), or Ruthenium Red (RR; 100 g/100 l). 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.
Document Type: Research Article
Affiliations: 1: Bioengineering 2: Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA 3: Physical Therapy 4: Department of Medicine, University of Minnesota, Lillehei Heart Institute, Minneapolis, MN, USA
Publication date: 2010-04-01