ArticleAmerican journal of physiology. Cell physiology2006
Acute hypoxia selectively inhibits KCNA5 channels in pulmonary artery smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 72 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Hypoxia and Multilineage Communication in 3D Organoids for Human Disease Modeling.Biomimetics (Basel, Switzerland) · 2025Review
- Pathophysiology and pathogenic mechanisms of pulmonary hypertension: role of membrane receptors, ion channels, and CaPhysiological reviews · 2023Review
- Hypoxia: molecular pathophysiological mechanisms in human diseases.Journal of physiology and biochemistry · 2022Review
- Review
- Halofuginone, a promising drug for treatment of pulmonary hypertension.British journal of pharmacology · 2021Article
- Genetic Delivery and Gene Therapy in Pulmonary Hypertension.International journal of molecular sciences · 2021Review
- On a Magical Mystery Tour with 8-Bromo-Cyclic ADP-Ribose: From All-or-None Block to Nanojunctions and the Cell-Wide Web.Molecules (Basel, Switzerland) · 2020Review
- Deciphering the evolutionary signatures of pinnipeds using novel genome sequences: The first genomes of Phoca largha, Callorhinus ursinus, and Eumetopias jubatus.Scientific reports · 2018Article
- BK channels in rat and human pulmonary smooth muscle cells are BKα-βPulmonary circulation · 2016Article
- AMP-activated protein kinase inhibits Kv 1.5 channel currents of pulmonary arterial myocytes in response to hypoxia and inhibition of mitochondrial oxidative phosphorylation.The Journal of physiology · 2016Article
- High-altitude Pulmonary Hypertension: an Update on Disease Pathogenesis and Management.The open cardiovascular medicine journal · 2016Article
- Polycomb-dependent repression of the potassium channel-encoding gene KCNA5 promotes cancer cell survival under conditions of stress.Oncogene · 2015Article
- Hypoxic pulmonary vasoconstriction, carotid body function and erythropoietin production in adult rats perinatally exposed to hyperoxia.The Journal of physiology · 2015Article
- Hitting the Bull's-Eye in Metastatic Cancers-NSAIDs Elevate ROS in Mitochondria, Inducing Malignant Cell Death.Pharmaceuticals (Basel, Switzerland) · 2015Review
- Chronic hypoxia selectively enhances L- and T-type voltage-dependent Ca2+ channel activity in pulmonary artery by upregulating Cav1.2 and Cav3.2.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Regulation of ion channels by pyridine nucleotides.Circulation research · 2013Review
- Dihydropyridine Ca(2+) channel blockers increase cytosolic [Ca(2+)] by activating Ca(2+)-sensing receptors in pulmonary arterial smooth muscle cells.Circulation research · 2013Article
- KCNA5 gene is not confirmed as a systemic sclerosis-related pulmonary arterial hypertension genetic susceptibility factor.Arthritis research & therapy · 2012Article
- Redox-sensitive sulfenic acid modification regulates surface expression of the cardiovascular voltage-gated potassium channel Kv1.5.Circulation research · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Acute hypoxia causes pulmonary vasoconstriction in part by inhibiting voltage-gated K(+) (Kv) channel activity in pulmonary artery smooth muscle cells (PASMC). The hypoxia-mediated decrease in Kv currents [I(K(V))] is selective to PASMC; hypoxia has little effect on I(K(V)) in mesenteric artery smooth muscle cells (MASMC). Functional Kv channels are homo- and/or heterotetramers of pore-forming alpha-subunits and regulatory beta-subunits. KCNA5 is a Kv channel alpha-subunit that forms functional Kv channels in PASMC and regulates resting membrane potential. We have shown that acute hypoxia selectively inhibits I(K(V)) through KCNA5 channels in PASMC. Overexpression of the human KCNA5 gene increased I(K(V)) and caused membrane hyperpolarization in HEK-293, COS-7, and rat MASMC and PASMC. Acute hypoxia did not affect I(K(V)) in KCNA5-transfected HEK-293 and COS-7 cells. However, overexpression of KCNA5 in PASMC conferred its sensitivity to hypoxia. Reduction of Po(2) from 145 to 35 mmHg reduced I(K(V)) by approximately 40% in rat PASMC transfected with human KCNA5 but had no effect on I(K(V)) in KCNA5-transfected rat MASMC (or HEK and COS cells). These results indicate that KCNA5 is an important Kv channel that regulates resting membrane potential and that acute hypoxia selectively reduces KCNA5 channel activity in PASMC relative to MASMC and other cell types. Because Kv channels (including KCNA5) are ubiquitously expressed in PASMC and MASMC, the observation from this study indicates that a hypoxia-sensitive mechanism essential for inhibiting KCNA5 channel activity is exclusively present in PASMC. The divergent effect of hypoxia on I(K(V)) in PASMC and MASMC also may be due to different expression levels of KCNA5 channels.
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