Stone Audrey J, Kaufman Marc P
Heart and Vascular Institute, Penn State College of Medicine, Hershey, PA 17033, United States.
Heart and Vascular Institute, Penn State College of Medicine, Hershey, PA 17033, United States.
Auton Neurosci. 2015 Mar;188:69-73. doi: 10.1016/j.autneu.2014.10.014. Epub 2014 Oct 22.
The exercise pressor reflex contributes to increases in cardiovascular and ventilatory function during exercise. These reflexive increases are caused by both mechanical stimulation and metabolic stimulation of group III and IV afferents with endings in contracting skeletal muscle. Patients with peripheral artery disease (PAD) have an augmented exercise pressor reflex. Recently, an animal model of PAD was established which allows further investigation of possible mechanisms involved in this augmented reflex. Earlier studies have identified ASIC3 channels, bradykinin receptors, P2X receptors, endoperoxide receptors, and thromboxane receptors as playing a role in evoking the exercise pressor reflex in healthy rats. This review focuses on recent studies using a rat model of PAD in order to determine possible mechanisms contributing to the exaggerated exercise pressor reflex seen in patients with this disease.
运动升压反射有助于运动期间心血管和通气功能的增强。这些反射性增强是由III类和IV类传入神经在收缩骨骼肌中的末梢受到机械刺激和代谢刺激共同引起的。外周动脉疾病（PAD）患者具有增强的运动升压反射。最近，建立了一种PAD动物模型，这使得能够进一步研究参与这种增强反射的可能机制。早期研究已确定ASIC3通道、缓激肽受体、P2X受体、内过氧化物受体和血栓素受体在健康大鼠诱发运动升压反射中发挥作用。本综述重点关注使用PAD大鼠模型的近期研究，以确定导致该病患者出现过度运动升压反射的可能机制。
