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Citations to this article

Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes.
S L Archer, … , H L Reeve, V Hampl
S L Archer, … , H L Reeve, V Hampl
Published June 1, 1998
Citation Information: J Clin Invest. 1998;101(11):2319-2330. https://doi.org/10.1172/JCI333.
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Research Article

Molecular identification of the role of voltage-gated K+ channels, Kv1.5 and Kv2.1, in hypoxic pulmonary vasoconstriction and control of resting membrane potential in rat pulmonary artery myocytes.

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Abstract

Hypoxia initiates pulmonary vasoconstriction (HPV) by inhibiting one or more voltage-gated potassium channels (Kv) in the pulmonary artery smooth muscle cells (PASMCs) of resistance arteries. The resulting membrane depolarization increases opening of voltage-gated calcium channels, raising cytosolic Ca2+ and initiating HPV. There are presently nine families of Kv channels known and pharmacological inhibitors lack the specificity to distinguish those involved in control of resting membrane potential (Em) or HPV. However, the Kv channels involved in Em and HPV have characteristic electrophysiological and pharmacological properties which suggest their molecular identity. They are slowly inactivating, delayed rectifier currents, inhibited by 4-aminopyridine (4-AP) but insensitive to charybdotoxin. Candidate Kv channels with these traits (Kv1.5 and Kv2.1) were studied. Antibodies were used to immunolocalize and functionally characterize the contribution of Kv1. 5 and Kv2.1 to PASMC electrophysiology and vascular tone. Immunoblotting confirmed the presence of Kv1.1, 1.2, 1.3, 1.5, 1.6, and 2.1, but not Kv1.4, in PASMCs. Intracellular administration of anti-Kv2.1 inhibited whole cell K+ current (IK) and depolarized Em. Anti-Kv2.1 also elevated resting tension and diminished 4-AP-induced vasoconstriction in membrane-permeabilized pulmonary artery rings. Anti-Kv1.5 inhibited IK and selectively reduced the rise in [Ca2+]i and constriction caused by hypoxia and 4-AP. However, anti-Kv1.5 neither caused depolarization nor elevated basal pulmonary artery tone. This study demonstrates that antibodies can be used to dissect the whole cell K+ currents in mammalian cells. We conclude that Kv2. 1 is an important determinant of resting Em in PASMCs from resistance arteries. Both Kv2.1 and Kv1.5 contribute to the initiation of HPV.

Authors

S L Archer, E Souil, A T Dinh-Xuan, B Schremmer, J C Mercier, A El Yaagoubi, L Nguyen-Huu, H L Reeve, V Hampl

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Total citations by year

Year: 2025 2024 2023 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1970 Total
Citations: 1 4 6 5 4 7 6 5 15 8 12 16 23 13 123 22 30 13 17 17 20 16 6 25 21 12 10 1 458
Citation information
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Citations to this article in year 2004 (16)

Title and authors Publication Year
Hypoxic pulmonary vasoconstriction in cardiothoracic surgery: basic mechanisms to potential therapies
BM Tsai, M Wang, MW Turrentine, Y Mahomed, JW Brown, DR Meldrum
The Annals of Thoracic Surgery 2004
Blunted effect of the Kv channel inhibitor on pulmonary circulation in Tibetan sheep: A model for studying hypoxia and pulmonary artery pressure regulation
T Ishizaki, A Sakai, T Koizumi, Z Ruan, ZG Wang
Respirology 2004
Molecular mechanisms underlying oxygen reception
EÉ Kolesnikova
Neurophysiology 2004
Cellular localization of Shab and Shaw potassium channels in the lobster stomatogastric ganglion
LB French, CC Lanning, M Matly, RM Harris-Warrick
Neuroscience 2004
Subacute Hypoxia Decreases Voltage-Activated Potassium Channel Expression and Function in Pulmonary Artery Myocytes
Z Hong, EK Weir, DP Nelson, A Olschewski
American journal of respiratory cell and molecular biology 2004
Selective expression of Kir6.1 protein in different vascular and non-vascular tissues
X Sun, K Cao, G Yang, Y Huang, ST Hanna, R Wang
Biochemical Pharmacology 2004
Functional up-regulation of KCNA gene family expression in murine mesenteric resistance artery smooth muscle: Resistance artery KCNA gene family expression
SJ Fountain, A Cheong, R Flemming, L Mair, A Sivaprasadarao, DJ Beech
The Journal of Physiology 2004
Direct block by bisindolylmaleimide of the voltage-dependent K+ currents of rat mesenteric arterial smooth muscle
A Kim, YM Bae, J Kim, B Kim, WK Ho, YE Earm, SI Cho
European Journal of Pharmacology 2004
Activation of K + channels: an essential pathway in programmed cell death
CV Remillard, JX Yuan
American journal of physiology. Lung cellular and molecular physiology 2004
Diversity of voltage-dependent K + channels in human pulmonary artery smooth muscle cells
O Platoshyn, CV Remillard, I Fantozzi, M Mandegar, TT Sison, S Zhang, E Burg, JX Yuan
American journal of physiology. Lung cellular and molecular physiology 2004
Overexpression of human KCNA5 increases IK(V) and enhances apoptosis
EE Brevnova, O Platoshyn, S Zhang, JX Yuan
American journal of physiology. Cell physiology 2004
Regulation of oxygen sensing by ion channels
J López-Barneo, R Toro, KL Levitsky, MD Chiara, P Ortega-Sáenz
Journal of applied physiology 2004
Hyperoxia causes oxygen free radical-mediated membrane injury and alters myocardial function and hemodynamics in the newborn
KS Bandali, MP Belanger, C Wittnich
American journal of physiology. Heart and circulatory physiology 2004
Calcium, mitochondria and oxygen sensing in the pulmonary circulation
JP Ward, VA Snetkov, PI Aaronson
Cell Calcium 2004
Hypoxic vasorelaxation: Ca2+-dependent and Ca2+-independent mechanisms
GD Thorne, Y Ishida, RJ Paul
Cell Calcium 2004
Why Potassium Channel Dysfunction May Be ‘Missing Link’ in Pathophysiology of PAH
ED Michelakis, SL Archer
Advances in Pulmonary Hypertension 2004

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