Endothelin-1 and the kidney - beyond BP

Neeraj Dhaun*, David J. Webb, David C. Kluth

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

Abstract / Description of output

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.

Original languageEnglish
Pages (from-to)720-731
Number of pages12
JournalBritish Journal of Pharmacology
Volume167
Issue number4
DOIs
Publication statusPublished - 1 Oct 2012

Keywords / Materials (for Non-textual outputs)

  • inflammation
  • BLOOD-PRESSURE
  • BP-independent
  • PODOCYTE INJURY
  • RENAL-DISEASE
  • LONG-TERM PROGNOSIS
  • chronic kidney disease
  • ETB-RECEPTOR
  • endothelin-1
  • ANGIOTENSIN-II
  • NITRIC-OXIDE
  • DUCT-SPECIFIC KNOCKOUT
  • A RECEPTOR ANTAGONISM
  • RAT MESANGIAL CELLS

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