Stocker Sean D, Kinsman Brian J, Sved Alan F
From the Department of Medicine, Renal-Electrolyte Division (S.D.S., B.J.K.), Department of Neuroscience (A.F.S.), and University of Pittsburgh Hypertension Center (S.D.S.), University of Pittsburgh, PA.
Hypertension. 2017 Jul 24. doi: 10.1161/HYPERTENSIONAHA.117.08936.
Neurally-mediated hypertension results from a dysregulation of sympathetic and/or neuroendocrine mechanisms to increase ABP. Multiple factors may exert multiple central effects to alter neural circuits and produce unique sympathetic signatures and elevate ABP. In this brief review, we have discussed novel observations regarding three contributing factors: dietary salt intake, obesity, and inflammation. However, the interaction among these and other factors is likely much more complex; recent studies suggest a prior exposure to one stimulus may sensitize the response to a subsequent hypertensive stimulus. Insight into the central mechanisms by which these factors selectively alter SNA or cooperatively interact to impact hypertension may represent a platform for novel therapeutic treatment strategies.
神经介导性高血压是由交感神经和/或神经内分泌机制失调导致动脉血压（ABP）升高引起的。多种因素可能产生多种中枢效应，改变神经回路，产生独特的交感神经特征并升高ABP。在这篇简短的综述中，我们讨论了关于三个促成因素的新观察结果：饮食盐摄入量、肥胖和炎症。然而，这些因素与其他因素之间的相互作用可能要复杂得多；最近的研究表明，先前暴露于一种刺激可能会使对随后的高血压刺激的反应敏感化。深入了解这些因素选择性改变交感神经活动（SNA）或协同相互作用以影响高血压的中枢机制，可能为新的治疗策略提供一个平台。
