The role of shear stress and sympathetic nervous activity in the regulation of human arterial function and structure

我们的动脉由一层叫做血管内皮的细胞构成。 由于它们位于动脉内侧，内皮细胞不断暴露于流动血液产生的摩擦力。 这种摩擦力被称为剪切力，在调节内皮细胞反应中起着关键作用，这些反应在短期和长期内改变动脉大小和硬度。 我们有兴趣了解内皮细胞对剪切应力变化的敏感性，其反应速度以及这些因素在手臂与腿部动脉中的差异。 我们将使用最先进的多普勒超声技术来测量剪切应力的变化以及动脉大小和刚度的变化。 在日常生活中，剪切应力增加的最常见原因是进行运动。 运动也会导致动脉功能和结构的长期变化，然而，我们不知道这些变化是否是由剪切应力本身的增加或其他随运动而变化的变量引起的。 我们将隔离的作用，在动脉功能的变化与一种新的技术，使我们能够模仿运动引起的变化，而不必进行收缩的剪切应力的剪切应力。 除了对剪切力的变化做出反应外，我们的动脉还受到神经的控制。 与刺激骨骼肌收缩的运动神经元类似，控制动脉的神经导致血管壁的肌肉收缩，使血管变小。 我们仍然没有清楚地了解，当在同一动脉中同时经历时，对剪切应力增加的反应和对神经信号的反应是如何相互作用的。 在实验中，我们将操纵这两个变量，并测量动脉大小和血液中反映神经和内皮细胞功能的因素的变化。 这将使我们深入了解动脉中信号的复杂相互作用和整合。 从这些研究中获得的信息将有助于促进我们对基本人类心血管功能的理解。

Our arteries are lined by a single layer of cells called the vascular endothelium. Due to their position on the inside of the artery, the endothelial cells are constantly exposed to the frictional force created by the flowing blood. Termed shear stress, this frictional force plays a key role in regulating endothelial cell responses that change artery size and stiffness in both the short and the long term. We are interested in understanding the sensitivity of the endothelium to changes in shear stress, the speed of its responses and how these factors may differ in arteries that are in the arms vs. the legs. We will use cutting edge Doppler ultrasound technology to measure both changes in shear stress and changes in artery size and stiffness. In daily living, the most common cause of increases in shear stress is performing exercise. Exercise also results in long term changes in artery function and structure, however, we do not know if these changes are brought about by increases in shear stress per se, or other variables that change with exercise. We will isolate the role of shear stress in changes in artery function with a novel technique that allows us to mimic exercise induced changes in shear stress without having to perform contractions. In addition to responding to changes in shear stress, our arteries are also controlled by nerves. Similar to the motor neurons that that stimulate our skeletal muscles to contract, the nerves that control our arteries cause the muscle in their walls to contract, making the vessel smaller. We still do not clearly understand the ways in which responses to increases in shear stress, and responses to signals from the nerves interact when they are experienced simultaneously in the same artery. In experiments we will manipulate both variables, and measure changes in artery size and factors in the blood that reflect neural and endothelial cell function. This will give us important insight into the complex interaction and integration of signals in our arteries. The information gained from these studies will assist in advancing our understanding of basic human cardiovascular function.