Thomas Gail D
Heart and Vascular Institute, Penn State College of Medicine, 500 University Drive, H047, Hershey, PA 17033, United States.
Auton Neurosci. 2015 Mar;188:64-8. doi: 10.1016/j.autneu.2014.10.019. Epub 2014 Oct 23.
Sympathetic vasoconstriction is normally attenuated in exercising muscle by local changes in muscle metabolites and other substances that reduce vascular responsiveness to α-adrenergic receptor activation. Termed functional sympatholysis, this protective mechanism is thought to optimize muscle blood flow distribution to match perfusion with metabolic demand. Emerging evidence from both animal and human studies indicate that functional sympatholysis is impaired in hypertension and may constitute an important underlying cause of skeletal muscle malperfusion during exercise in this common cardiovascular condition. Findings from studies of animal models of hypertension and patients with essential hypertension will be integrated in this review to provide insight into the underlying mechanisms responsible for inappropriate sympathetic vasoconstriction in exercising muscle and the treatment options that may restore functional sympatholysis and improve muscle perfusion during exercise.
在运动的肌肉中，交感神经血管收缩通常会因肌肉代谢产物和其他物质的局部变化而减弱，这些物质会降低血管对α-肾上腺素能受体激活的反应性。这种被称为功能性交感神经抑制的保护机制被认为可优化肌肉血流分布，使灌注与代谢需求相匹配。来自动物和人体研究的新证据表明，高血压患者存在功能性交感神经抑制受损的情况，这可能是这种常见心血管疾病患者运动期间骨骼肌灌注不良的一个重要潜在原因。本文将整合高血压动物模型和原发性高血压患者的研究结果，以深入了解运动肌肉中交感神经血管收缩异常的潜在机制，以及可能恢复功能性交感神经抑制并改善运动期间肌肉灌注的治疗选择。
