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肾脏近曲小管内血管紧张素II在高血压发病机制研究的最新进展

发布日期:2017-04-13    浏览次数:

学   术   报   告

 

题   目:肾脏近曲小管内血管紧张素II在高血压发病机制研究的最新进展

报告人 ZHUO, JIA LONG (卓家隆)   

Professor and Director, Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology, The University of Mississippi Medical Center

时   间2017417(星期一)16: 00-17:00

地   点:逸夫楼310

                                 基础医学院中西医结合学系

研究生可计学术活动学分

 

 

简介

Dr. Zhuo is best known as one of very few scientists, who has devoted the entire career to studying the localization and roles of circulating (endocrine), tissue (paracrine), and intracellular (intracrine) renin-angiotensin system (RAS) in the kidney, with more than 100 original and invited review publications and book chapters mostly in the RAS research. In late 1980s, Zhuo was a pioneer in advancing the concept that ANG II and atrial natriuretic factor (ANF) regulate proximal tubule glomerulotubular balance in the kidney. In 1990s, Zhuo and his colleagues had made seminal contributions to systematically mapping the localization of ACE, ANG II receptors (AT1, AT2 and AT4), bradykinin B2 receptors, and endothelin ETA and ETB receptors in the glomeruli, proximal tubules, and renomedullary interstitial cells in the medulla of the kidney using state of the art quantitative in vitro and in vivo light and electron microscopic autoradiography. During the early 2000s, Zhuo and colleagues mechanistically demonstrated that circulating ANG II was taken up by the proximal tubule of the kidney via AT1 (AT1a) receptor-mediated mechanism, and that internalized ANG II acted as an intracrine peptide to regulate proximal tubular Na+ reabsorption and blood pressure. Most recently, Zhuo’s group was among the 1st to demonstrate that overexpression of an intracellular cyan fluorescent ANG II fusion protein selectively in the proximal tubule of the kidney using the proximal tubule-specific Sglt2 promoter elevated blood pressure via AT1 (AT1a)- and the Na+/H+ exchanger 3 (NHE3)-dependent mechanisms. Finally, Zhuo’s group has recently made seminal contributions to our understanding of the important role of NHE3 as a potential mediator of ANG II-induced hypertension and a regulator of pressure-natriuresis responses.