Open AccessFluid flow facilitates inward rectifier K+ current by convectively restoring [K+] at the cell membrane surface
Author(s) -
Jae Gon Kim,
Sang Woong Park,
Doyoung Byun,
Wahn Soo Choi,
Dong Jun Sung,
KyeongCheol Shin,
Hyunji Kim,
Young-Eun Leem,
JongSun Kang,
Hanna Cho,
Bokyung Kim,
Sung I Cho,
Young Min Bae
Publication year - 2016
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/srep39585
Subject(s) - biophysics , fluid dynamics , patch clamp , chemistry , extracellular , inward rectifier potassium ion channel , extracellular fluid , ion channel , mechanics , biology , physics , biochemistry , receptor
The inward rectifier Kir2.1 current (IKir2.1) was reported to be facilitated by fluid flow. However, the mechanism underlying this facilitation remains uncertain. We hypothesized that during K + influx or efflux, [K + ] adjacent to the outer mouth of the Kir2.1 channel might decrease or increase, respectively, compared with the average [K + ] of the bulk extracellular solution, and that fluid flow could restore the original [K + ] and result in the apparent facilitation of IKir2.1. We recorded the IKir2.1 in RBL-2H3 cells and HEK293T cells that were ectopically over-expressed with Kir2.1 channels by using the whole-cell patch-clamp technique. Fluid-flow application immediately increased the IKir2.1, which was not prevented by either the pretreatment with inhibitors of various protein kinases or the modulation of the cytoskeleton and caveolae. The magnitudes of the increases of IKir2.1 by fluid flow were driving force-dependent. Simulations performed using the Nernst-Planck mass equation indicated that [K + ] near the membrane surface fell markedly below the average [K + ] of the bulk extracellular solution during K + influx, and, notably, that fluid flow restored the decreased [K + ] at the cell surface in a flow rate-dependent manner. These results support the “convection-regulation hypothesis” and define a novel interpretation of fluid flow-induced modulation of ion channels.