Shear Stress Regulates the Endothelial Kir2.1 Ion Channel

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...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2002-05, Vol.99 (11), p.7780-7785
Main Authors: Hoger, Jeff H., Ilyin, Victor I., Forsyth, Scott, Hoger, Anne
Format: Article
Language:English
Subjects:
Amiloride - pharmacology
Amino Acid Substitution
Anatomy & physiology
Animals
Biological Sciences
Blood vessels
Cattle
Cell Line
Cell Membrane - drug effects
Cell Membrane - physiology
Cell membranes
Cells
Cells, Cultured
Egtazic Acid - pharmacology
Electric current
Electric potential
Endothelium, Vascular - physiology
Female
Humans
Ion channels
Ion currents
Ions
Mammals
Membrane Potentials - drug effects
Membrane Potentials - physiology
Messenger RNA
Mutagenesis, Site-Directed
Neomycin - pharmacology
Oocytes
Phosphorylation
Pipettes
Potassium - physiology
Potassium Channels, Inwardly Rectifying - chemistry
Potassium Channels, Inwardly Rectifying - genetics
Potassium Channels, Inwardly Rectifying - physiology
Recombinant Proteins - chemistry
Recombinant Proteins - metabolism
Shear stress
Stress, Mechanical
Transfection
Xenopus laevis
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Summary: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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.102184999