The TRPv1 receptor is a mediator of the exercise pressor reflex in rats.
The TRPv1 receptor is a mediator of the exercise pressor reflex in rats.
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TRPv1 受体是大鼠运动升压反射的介质。
DOI：
10.1113/jphysiol.2009.184952
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Garry,MaryG
中科院分区：
文献类型：
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作者：
Smith,ScottA;Leal,AnnaK;Williams,MauriceA;Murphy,MeganN;Mitchell,JereH;Garry,MaryG
骨骼肌运动加压反射(EPR)在体力活动中引起心率(HR)和平均动脉压(MAP)的增加。这种反射在收缩过程中通过刺激传入纤维而被激活，这些传入纤维响应于机械变形和/或骨骼肌工作的代谢副产物。负责激活这些传入神经元的分子机制尚未确定。有报道称，骨骼肌(定位于无髓传入纤维)中的瞬时受体电位香草素1(TRPV1)受体的激活引起MAP和HR的增加，这与EPR所产生的结果相似。因此，我们假设在肌肉收缩过程中刺激TRPV1受体有助于EPR的激活。去脑SD大鼠(n=61)在给予TRPV1受体拮抗剂卡萨西平(Capsazepine，100μg/100μL)、碘化铁角毒素(IRTX，1μg/100μL)或钌红(Ru Red，RR；100μg/100μL)前后，通过电诱导后肢静态肌肉收缩来激活EPR。单纯静力性肌肉收缩可引起HR(8±2次/分)和MAP(21±3 mm Hg)的增加。给予卡铂(2±1次/分；7±1毫米汞柱)、IRTX(3±2次/分；5±3毫米汞柱)和RR(0±1次/分；5±2毫米汞柱)后，心率和平均动脉压收缩反应显著降低(P<；0.05)。这些数据表明，在大鼠骨骼肌收缩过程中，TRPV1受体对EPR的激活起重要作用。
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 μg/100 μl), iodoresinaferatoxin (IRTX; 1 μg/100 μl), or Ruthenium Red (RR; 100 μg/100 μl). 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.