Applied laminar shear stress induced a K+ ion current in cells expressing the endothelial Kir2.1 channel, a response that was specifically prevented by tyrosine kinase inhibition.
Does applied fluid shear stress induce a K(+) ion current in cells expressing the endothelial Kir2.1 channel?
The study identifies the Kir2.1 channel as an early component of the endothelial shear response mechanism, which is regulated by tyrosine kinase.
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.
Hoger et al. (Tue,) conducted a other in Endothelial shear stress response. Laminar shear stress vs. No flow (stationary conditions) was evaluated on K+ shear current (IKS) amplitude. Applied laminar shear stress induced a K+ ion current in cells expressing the endothelial Kir2.1 channel, a response that was specifically prevented by tyrosine kinase inhibition.