Regulation of the Na-K-Cl co-transporter by the AMP-activated protein kinase

AMP 激活蛋白激酶对 Na-K-Cl 协同转运蛋白的调节

• 批准号: nhmrc : 156710
• 负责人: Prof David Power
• 金额: $ 15.14万
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2001
• 资助国家: 澳大利亚
• 起止时间: 2001-01-01 至 2003-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/regulation-na-k-protein-kinase/81903
• 关键词: Regulation; Na; Cl; co; transporter

The failure of the kidney to excrete enough salt is a major driving force behind high blood pressure, kidney failure and heart disease. At present, it is not known, in any detail, how the kidney is able to recognise that it is not excreting enough salt and how it changes the amount it excretes. This is important if, for example, someone eats a salty meal. Unless the kidney recognises that there is an excess of salt and adjusts itself to excrete it, then salt accumulates leading to high blood pressure, kidney and cardiac problems. In this study, we have identified a new mechanism that the kidney uses to detect salt and to excrete it. This could be a major advance in our understanding of high blood pressure and other common diseases.

肾脏不能排出足够的盐是高血压、肾衰竭和心脏病的主要驱动力。目前，尚不清楚肾脏如何识别其没有排泄足够的盐以及如何改变其排泄量。这是很重要的，例如，如果有人吃咸的食物。除非肾脏认识到有过量的盐，并调整自己排出它，然后盐积累导致高血压，肾脏和心脏问题。在这项研究中，我们发现了一种新的机制，肾脏利用这种机制来检测盐并将其排出体外。这可能是我们对高血压和其他常见疾病的理解的一个重大进展。