Hurr Chansol, Young Colin N
Department of Pharmacology and Physiology, School of Medicine and Health Sciences, The George Washington University, 2300 Eye Street NW, 448 Ross Hall, Washington, D.C., 20037, USA.
Curr Hypertens Rep. 2016 Apr;18(4):30. doi: 10.1007/s11906-016-0635-8.
Hypertension affects over 25 % of the population with the incidence continuing to rise, due in part to the growing obesity epidemic. Chronic elevations in sympathetic nerve activity (SNA) are a hallmark of the disease and contribute to elevations in blood pressure through influences on the vasculature, kidney, and heart (i.e., neurogenic hypertension). In this regard, a number of central nervous system mechanisms and neural pathways have emerged as crucial in chronically elevating SNA. However, it is important to consider that "sympathetic signatures" are present, with differential increases in SNA to regional organs that are dependent upon the disease progression. Here, we discuss recent findings on the central nervous system mechanisms and autonomic regulatory networks involved in neurogenic hypertension, in both non-obesity- and obesity-associated hypertension, with an emphasis on angiotensin-II, salt, oxidative and endoplasmic reticulum stress, inflammation, and the adipokine leptin.
高血压影响着超过25%的人口,且发病率持续上升,部分原因是肥胖流行日益严重。交感神经活动(SNA)的慢性升高是该疾病的一个标志,并通过对血管系统、肾脏和心脏的影响导致血压升高(即神经源性高血压)。在这方面,一些中枢神经系统机制和神经通路已成为慢性升高SNA的关键因素。然而,需要考虑的是存在“交感神经特征”,即SNA对不同区域器官的增加存在差异,这取决于疾病进展情况。在此,我们讨论近期关于神经源性高血压(包括非肥胖相关和肥胖相关高血压)中涉及的中枢神经系统机制和自主调节网络的研究发现,重点关注血管紧张素II、盐、氧化和内质网应激、炎症以及脂肪因子瘦素。