Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Am J Physiol Regul Integr Comp Physiol. 2013 Jul 15;305(2):R104-6. doi: 10.1152/ajpregu.00209.2013. Epub 2013 May 15.
The renin-angiotensin system (RAS) has long been established as one of the major mechanisms of hypertension through the increased levels of angiotensin (ANG) II and its resulting effect on the sympathetic nerve activity, arterial vasoconstriction, water reabsorption, and retention, etc. In the central nervous system, RAS activation affects body fluid homeostasis through increases in sympathetic nerve activity, water intake, food intake, and arginine vasopressin secretion. Previous studies, however, have shown that ANG II can be made in the brain, and it could possibly be through a new component called the (pro)renin receptor. This review intends to summarize the central and peripheral effects of the PRR on body fluid homeostasis.
肾素-血管紧张素系统（RAS）通过增加血管紧张素（ANG）II 的水平及其对交感神经活性、动脉血管收缩、水重吸收和保留等的影响，长期以来一直被认为是高血压的主要机制之一。在中枢神经系统中，RAS 的激活通过增加交感神经活性、水摄入、食物摄入和精氨酸加压素分泌来影响体液平衡。然而，先前的研究表明，ANG II 可以在大脑中产生，并且可能是通过一种叫做（前）肾素受体的新成分。本综述旨在总结 PRR 对体液平衡的中枢和外周作用。
