J Clin Invest. 2014 Jun;124(6):2341-7. doi: 10.1172/JCI72274. Epub 2014 Jun 2.
An essential link between the kidney and blood pressure control has long been known. Here, we review evidence supporting the premise that an impaired capacity of the kidney to excrete sodium in response to elevated blood pressure is a major contributor to hypertension, irrespective of the initiating cause. In this regard, recent work suggests that novel pathways controlling key sodium transporters in kidney epithelia have a critical impact on hypertension pathogenesis, supporting a model in which impaired renal sodium excretion is a final common pathway through which vascular, neural, and inflammatory responses raise blood pressure. We also address recent findings calling into question long-standing notions regarding the relationship between sodium intake and changes in body fluid volume. Expanded understanding of the role of the kidney as both a cause and target of hypertension highlights key aspects of pathophysiology and may lead to identification of new strategies for prevention and treatment.
长期以来，人们一直知道肾脏和血压控制之间存在着重要联系。在这里，我们回顾了支持这一前提的证据，即肾脏排出钠的能力受损，无法应对血压升高，这是高血压的一个主要原因，而不论其起始原因是什么。在这方面，最近的研究表明，控制肾脏上皮细胞中关键钠转运体的新途径对高血压的发病机制有重大影响，支持这样一种模式，即肾脏排钠能力受损是血管、神经和炎症反应升高血压的共同最终途径。我们还讨论了最近的一些发现，这些发现对钠摄入量与体液量变化之间关系的长期观念提出了质疑。对肾脏作为高血压的原因和靶器官的作用的理解的扩展突出了病理生理学的关键方面，并可能导致确定新的预防和治疗策略。
