Aldosterone-induced signalling and cation transport in the distal nephron

Steroids. 2008 Oct;73(9-10):979-84. doi: 10.1016/j.steroids.2008.01.013. Epub 2008 Jan 19.

Abstract

Aldosterone is an important regulator of Na(+) and K(+) transport in the distal nephron modulating the surface expression of transporters through the action of the mineralocorticoid receptor as a ligand-dependent transcription factor. Aldosterone stimulates the rapid activation of protein kinase-based signalling cascades that modulate the genomic effects of the hormone. Evidence is accumulating about the multi-factorial regulation of the epithelial sodium channel (ENaC) by aldosterone. Recent published data suggests that the activation of a novel PKC/PKD signalling pathway through the c-Src-dependent trans-activation of epidermal growth factor receptor contributes to early ENaC trafficking in response to aldosterone.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aldosterone / metabolism*
  • Animals
  • Biological Transport
  • Cations*
  • Cell Communication
  • Enzyme Activation
  • Epidermal Growth Factor / metabolism
  • Humans
  • Ion Transport
  • Models, Biological
  • Nephrons / metabolism*
  • Potassium / chemistry
  • Protein Kinases / metabolism
  • Signal Transduction
  • Transcriptional Activation

Substances

  • Cations
  • Aldosterone
  • Epidermal Growth Factor
  • Protein Kinases
  • Potassium