Endothelin-1 and the kidney – beyond BP

Authors

  • Neeraj Dhaun,

    Corresponding author
    1. Department of Renal Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK
    2. Cardiovascular Sciences, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK
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  • David J Webb,

    1. Cardiovascular Sciences, The Queen's Medical Research Institute, University of Edinburgh, Edinburgh, UK
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  • David C Kluth

    1. Department of Renal Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK
    2. Centres for Inflammation Research
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Dr Neeraj Dhaun, The Queen's Medical Research Institute, 3rd Floor East, Room E3.23, 47 Little France Crescent, Edinburgh EH16 4TJ, UK. E-mail: bean.dhaun@ed.ac.uk

Abstract

Since its discovery over 20 years ago endothelin-1 (ET-1) has been implicated in a number of physiological and pathophysiological processes. Its role in the development and progression of chronic kidney disease (CKD) is well established and is an area of ongoing intense research. There are now available a number of ET receptor antagonists many of which have been used in trials with CKD patients and shown to reduce BP and proteinuria. However, ET-1 has a number of BP-independent effects. Importantly, and in relation to the kidney, ET-1 has clear roles to play in cell proliferation, podocyte dysfunction, inflammation and fibrosis, and arguably, these actions of ET-1 may be more significant in the progression of CKD than its prohypertensive actions. This review will focus on the potential role of ET-1 in renal disease with an emphasis on its BP-independent actions.

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