The exercise pressor reflex is a neural control mechanism responsible for the cardiovascular responses to exercise. As exercise is initiated, thin fiber muscle afferent nerves are activated by mechanical and metabolic stimuli arising in the contracting muscles. This leads to reflex increases in arterial blood pressure and heart rate primarily through activation of sympathetic nerve activity (SNA). Studies of humans and animals have indicated that the exercise pressor reflex is exaggerated in a number of cardiovascular diseases. For the last several years, a series of studies have employed a rodent model to examine the mechanisms at receptor and cellular levels by which responses of SNA and blood pressure to static exercise are heightened in peripheral artery disease (PAD), one of the most common cardiovascular disorders. Specifically, femoral artery occlusion is used to study intermittent claudication that is observed in human PAD. Our studies have demonstrated that the receptors on thin fiber muscle afferents including transient receptor potential vanilloid type 1 (TRPV1), purinergic P2X3 and acid sensing ion channel subtype 3 (ASIC3) are engaged in augmented autonomic responses this disease. This review will present some of recent results in regard with several receptors in muscle sensory neurons in contribution to augmented autonomic responses in PAD. We will emphasize the role played by nerve growth factor (NGF) in regulating those sensory receptors in the processing of amplified exercise pressor reflex. Also, we will discuss the role played by hypoxia-inducible facor-1α regarding the enhanced autonomic reflex with femoral artery occlusion. The purpose of this review is to focus on a theme namely that PAD accentuates reflexively autonomic responses to exercise and further address regulatory mechanisms leading to abnormal autonomic responsiveness.
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号