Abstract:
: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.
journal_name
Proc Natl Acad Sci U S Aauthors
Hoger JH,Ilyin VI,Forsyth S,Hoger Adoi
10.1073/pnas.102184999keywords:
subject
Has Abstractpub_date
2002-05-28 00:00:00pages
7780-5issue
11eissn
0027-8424issn
1091-6490journal_volume
99pub_type
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