作者: Scott A. Smith , Anna K. Leal , Maurice A. Williams , Megan N. Murphy , Jere H. Mitchell
DOI: 10.1113/JPHYSIOL.2009.184952
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摘要: The skeletal muscle exercise pressor reflex (EPR) induces increases in heart rate (HR) and mean arterial pressure (MAP) during physical activity. This is activated contraction by stimulation of afferent fibres responsive to mechanical distortion and/or the metabolic by-products work. molecular mechanisms responsible for activating these neurons have yet be identified. It has been reported that activation transient receptor potential vanilloid 1 (TRPv1) within (localized unmyelinated fibres) elicits MAP HR similar those generated EPR. Thus, we hypothesized TRPv1 contributes EPR was electrically induced static hindlimb decerebrate Sprague–Dawley rats (n= 61) before after administration antagonists, capsazepine (Capz; 100 μg/100 μl), iodoresinaferatoxin (IRTX; or Ruthenium Red (RR; μl). Static alone both (8 ± 2 bpm) (21 3 mmHg). responses were significantly lower (P < 0.05) Capz (2 bpm; 7 mmHg, respectively), IRTX (3 5 respectively) RR (0 1, respectively). These data suggest importantly rat.