Shear stress regulates the endothelial Kir2.1 ion channel

Proc Natl Acad Sci U S A. 2002 May 28;99(11):7780-5. doi: 10.1073/pnas.102184999.


Endothelial cells (ECs) line the mammalian vascular system and respond to the hemodynamic stimulus of fluid shear stress, the frictional force produced by blood flow. When ECs are exposed to shear stress, one of the fastest responses is an increase of K(+) conductance, which suggests that ion channels are involved in the early shear stress response. Here we show that an applied shear stress induces a K(+) ion current in cells expressing the endothelial Kir2.1 channel. This ion current shares the properties of the shear-induced current found in ECs. In addition, the shear current induction can be specifically prevented by tyrosine kinase inhibition. Our findings identify the Kir2.1 channel as an early component of the endothelial shear response mechanism.

Publication types

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

MeSH terms

  • Amiloride / pharmacology
  • Amino Acid Substitution
  • Animals
  • Cattle
  • Cell Line
  • Cell Membrane / drug effects
  • Cell Membrane / physiology
  • Cells, Cultured
  • Egtazic Acid / pharmacology
  • Endothelium, Vascular / physiology*
  • Female
  • Humans
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Mutagenesis, Site-Directed
  • Neomycin / pharmacology
  • Phosphorylation
  • Potassium / physiology
  • Potassium Channels, Inwardly Rectifying / chemistry
  • Potassium Channels, Inwardly Rectifying / genetics
  • Potassium Channels, Inwardly Rectifying / physiology*
  • Recombinant Proteins / chemistry
  • Recombinant Proteins / metabolism
  • Stress, Mechanical
  • Transfection
  • Xenopus laevis


  • Potassium Channels, Inwardly Rectifying
  • Recombinant Proteins
  • Egtazic Acid
  • Amiloride
  • Neomycin
  • Potassium