Division of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers , Durham, North Carolina.
Antioxid Redox Signal. 2014 Jan 1;20(1):102-20. doi: 10.1089/ars.2013.5258. Epub 2013 Apr 19.
Innate and adaptive immunity play fundamental roles in the development of hypertension and its complications. As effectors of the cell-mediated immune response, myeloid cells and T lymphocytes protect the host organism from infection by attacking foreign intruders with bursts of reactive oxygen species (ROS).
While these ROS may help to preserve the vascular tone and thereby protect against circulatory collapse in the face of overwhelming infection, aberrant elaboration of ROS triggered by immune cells in the absence of a hemodynamic insult can lead to pathologic increases in blood pressure. Conversely, misdirected oxidative stress in cardiovascular control organs, including the vasculature, the kidney, and the nervous system potentiates inflammatory responses, augmenting blood pressure elevation and inciting target organ damage.
Inflammation and oxidative stress thereby act as cooperative and synergistic partners in the pathogenesis of hypertension.
Pharmacologic interventions for hypertensive patients will need to exploit this robust bidirectional relationship between ROS generation and immune activation in cardiovascular control organs to maximize therapeutic benefit, while limiting off-target side effects.
先天免疫和适应性免疫在高血压及其并发症的发展中起着根本作用。作为细胞介导免疫反应的效应物，髓样细胞和 T 淋巴细胞通过产生大量的活性氧物质 (ROS) 来攻击外来入侵者，从而保护宿主免受感染。
虽然这些 ROS 有助于维持血管张力，从而防止在面临压倒性感染时循环崩溃，但免疫细胞在没有血流冲击的情况下产生的异常 ROS 会导致病理性血压升高。相反，心血管控制器官（包括血管、肾脏和神经系统）中定向错误的氧化应激会增强炎症反应，增加血压升高并引发靶器官损伤。
因此，炎症和氧化应激在高血压的发病机制中是协同和协同的伙伴。
高血压患者的药物治疗干预措施需要利用心血管控制器官中 ROS 生成和免疫激活之间这种强大的双向关系，以最大限度地提高治疗效果，同时限制非靶向副作用。
