颈动脉体研究的主要进展：过去与现在。

文献信息

中文摘要

背景： 颈动脉体（CB）在18世纪被解剖学描述，到20世纪初，它已被确立为主要的外周化学感受器，感受动脉血Po2、Pco2和[H+]，从而介导心肺反射反应。然而，缺乏现代电生理和分子技术限制了对刺激转导机制的认识。几十年来，研究主要围绕O2和CO2-H+感受机制以及假定的兴奋性递质如多巴胺、乙酰胆碱和ATP的作用等未解决的争论。这些不确定性反映了整合生理学与分子机制之间的重大差距。自20世纪80年代末以来，情况发生了很大变化。电生理、分子和遗传学研究表明，球细胞中的O2感受取决于线粒体氧化代谢产生的代谢信号与细胞膜K+通道活动之间的耦合。在过去20年中，越来越多的证据强调了CB在自主神经相关疾病中的新作用。异常的CB化学感受过度活跃已成为自主神经功能障碍的主动驱动因素，其特征是在心力衰竭、阻塞性睡眠呼吸暂停、严重高血压和代谢改变等情况下出现交感神经兴奋。在这篇综述中，我们将分析CB研究的主要进展以及从被动传感器到交感神经介导的心血管代谢疾病关键贡献者的概念转变。

英文摘要

The carotid body (CB) was anatomically described in the 18th century, and by the early 20th century, it was established as the principal peripheral chemoreceptor that senses arterial blood Po2, Pco2, and [H+], thereby mediating cardiorespiratory reflex responses. However, the absence of modern electrophysiological and molecular techniques limited the mechanistic insight into stimulus transduction. For decades, the research was dominated by unresolved debates over the mechanisms underlying O2 and CO2-H+ sensing and the role of putative excitatory transmitters such as dopamine, acetylcholine, and ATP. These uncertainties reflected a major gap between integrative physiology and molecular mechanisms. Since the late 1980s, the situation has changed considerably. Electrophysiological, molecular, and genetic studies have shown that O2 sensing in glomus cells depends on the coupling between metabolic signals derived from the mitochondrial oxidative metabolism and K+ channels activity in the cell membrane. Over the past 20 years, a growing body of evidence has highlighted a novel role for the CB in autonomic-related diseases. An abnormal CB chemosensory overactivity has emerged as an active driver for autonomic dysfunction, featured by sympathetic excitation in conditions such as heart failure, obstructive sleep apnea, severe hypertension, and metabolic alterations. In this review, we will analyze major advances in CB research and the conceptual change from a passive sensor to a key contributor to sympathetic-mediated cardiometabolic diseases.