Antagonism of the TRPv1 receptor partially corrects muscle metaboreflex overactivity in spontaneously hypertensive rats.
Antagonism of the TRPv1 receptor partially corrects muscle metaboreflex overactivity in spontaneously hypertensive rats.
复制标题
TRPv1 受体的拮抗作用可部分纠正自发性高血压大鼠的肌肉代谢反射过度活动。
DOI：
10.1113/jphysiol.2011.214429
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发表时间：
2011
期刊：
影响因子：
--
通讯作者：
Smith,ScottA
中科院分区：
文献类型：
--
作者：
Mizuno,Masaki;Murphy,MeganN;Mitchell,JereH;Smith,ScottA
非技术性总结高血压患者对运动的心血管反应被夸大。这种提高的循环反应性增加了在运动期间和运动后立即发生不良心血管事件的风险。越来越多的证据表明，肌肉代谢反射，一种起源于骨骼肌的化学敏感性外周反射，对这种运动引起的异常心血管反应有重要作用。然而，它的作用仍然存在争议。此外，高血压代谢反射功能障碍的受体机制仍不确定。为此，目前的研究表明，代谢反射是过度活跃的高血压大鼠引起夸张的增加交感神经活动和血压。重要的是，这项研究首次表明，高血压中表现出的代谢反射功能障碍部分是由骨骼肌TRPv1受体的激活介导的。因此，这项研究确定了肌肉代谢反射，特别是TRPv1受体，作为治疗高血压运动期间心血管兴奋过度的潜在靶点。
Non‐technical summaryThe cardiovascular response to exercise is exaggerated in hypertension. This heightened circulatory responsiveness increases the risk of occurrence of an adverse cardiovascular event during and immediately following a bout of exercise. Accumulating evidence suggests the muscle metaboreflex, a chemically sensitive peripheral reflex originating in skeletal muscle, contributes significantly to this abnormal cardiovascular response to exercise. However, its role remains controversial. In addition, the receptor mechanisms underlying metaboreflex dysfunction in hypertension remain undetermined. To this end, the current investigation demonstrates that the metaboreflex is overactive in hypertensive rats eliciting exaggerated increases in sympathetic nerve activity and blood pressure. Importantly, the study shows, for the first time, that the metaboreflex dysfunction manifest in hypertension is mediated, in part, by activation of the skeletal muscle TRPv1 receptor. As such, the investigation identifies the muscle metaboreflex, specifically the TRPv1 receptor, as a potential target for the treatment of cardiovascular hyperexcitability during exercise in hypertension.