Campese Vito M, Park Jeanie
Division of Nephrology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
J Nephrol. 2006 Nov-Dec;19(6):691-8.
The crucial role of the kidneys in regulation of systemic blood pressure has been known for more than 70 years. A multitude of studies have described the regulatory mechanisms behind this interaction, and elucidate why kidney disease is such a rampant and difficult form of secondary hypertension. Historically, renal hypertension has primarily been described as derangements of the renin-angiotensin-aldosterone system (RAAS), and salt and volume retention. Renally mediated hypertension involves the activation of RAAS leading to angiotensin II-mediated vaso-constriction, and aldosterone-mediated salt retention. The increased sodium retention and volume expansion seen in kidney disease is accompanied by a failure to autoregulate the peripheral vasculature, leading to hypertension. An-giotensin II and aldosterone also cause increased inflammation and endothelial dysfunction, and volume retention leads to the elaboration of ouabain-like compounds that contribute to increased total peripheral resistance. More recently, studies have shown that activation of renal afferent pathways connecting with specific brain nuclei involved in the noradrenergic control of blood pressure appears to play a substantial role. This article will review the classic pa-radigms, as well as new and emerging paradigms linking the kidney with blood pressure.
肾脏在调节全身血压方面的关键作用已为人所知70多年。众多研究描述了这种相互作用背后的调节机制，并阐明了为什么肾脏疾病是继发性高血压如此常见且难以治疗的一种形式。从历史上看，肾性高血压主要被描述为肾素-血管紧张素-醛固酮系统（RAAS）紊乱以及盐和容量潴留。肾介导的高血压涉及RAAS的激活，导致血管紧张素II介导的血管收缩以及醛固酮介导的盐潴留。在肾脏疾病中出现的钠潴留增加和容量扩张伴随着外周血管系统自身调节功能的失效，从而导致高血压。血管紧张素II和醛固酮还会导致炎症增加和内皮功能障碍，而容量潴留会导致类哇巴因化合物的产生，这会导致总外周阻力增加。最近的研究表明，与参与血压去甲肾上腺素能控制的特定脑核相连的肾传入通路的激活似乎起着重要作用。本文将回顾将肾脏与血压联系起来的经典范式以及新出现的范式。
