ArticleBasic & clinical pharmacology & toxicology2013
Alterations of N-3 polyunsaturated fatty acid-activated K2P channels in hypoxia-induced pulmonary hypertension.
Article in Basic & clinical pharmacology & toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The Potential Role of Calcium Channels in Pulmonary Hypertension.BioMed research international · 2026Review
- Structure of the human TWIK-2 potassium channel and its inhibition by pimozide.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Impact of aging on vascular ion channels: perspectives and knowledge gaps across major organ systems.American journal of physiology. Heart and circulatory physiology · 2023Review
- Negative Influence by the Force: Mechanically Induced Hyperpolarization via KInternational journal of molecular sciences · 2021Review
- Aging Affects KFrontiers in physiology · 2021Article
- Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling.Antioxidants (Basel, Switzerland) · 2020Review
- A Single Simulated Heliox Dive Modifies Endothelial Function in the Vascular Wall of ApoE Knockout Male Rats More Than Females.Frontiers in physiology · 2019Article
- Implications of dietary ω-3 and ω-6 polyunsaturated fatty acids in breast cancer.Experimental and therapeutic medicine · 2018Article
- Hemodynamic and Pathologic Characterization of the TASK-1Frontiers in medicine · 2017Article
- Inhibition of Intermediate-Conductance Calcium-Activated K Channel (KCa3.1) and Fibroblast Mitogenesis by α-Linolenic Acid and Alterations of Channel Expression in the Lysosomal Storage Disorders, Fabry Disease, and Niemann Pick C.Frontiers in physiology · 2017Article
- Vascular Reactivity Profile of Novel KCa 3.1-Selective Positive-Gating Modulators in the Coronary Vascular Bed.Basic & clinical pharmacology & toxicology · 2016Article
- In-Depth Study of the Interaction, Sensitivity, and Gating Modulation by PUFAs on KFrontiers in physiology · 2016Review
- TWIK-2 channel deficiency leads to pulmonary hypertension through a rho-kinase-mediated process.Hypertension (Dallas, Tex. : 1979) · 2014Article
- Modulation of K(Ca)3.1 channels by eicosanoids, omega-3 fatty acids, and molecular determinants.PloS one · 2014Article
- The mechanism of ions in pulmonary hypertension.Pulmonary circulationReview
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Polyunsaturated fatty acid (PUFA)-activated two-pore domain potassium channels (K2P ) have been proposed to be expressed in the pulmonary vasculature. However, their physiological or pathophysiological roles are poorly defined. Here, we tested the hypothesis that PUFA-activated K2P are involved in pulmonary vasorelaxation and that alterations of channel expression are pathophysiologically linked to pulmonary hypertension. Expression of PUFA-activated K2P in the murine lung was investigated by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), by patch clamp (PC) and myography. K2P -gene expression was examined in chronic hypoxic mice. qRT-PCR showed that the K2P 2.1 and K2P 6.1 were the predominantly expressed K2P in the murine lung. IHC revealed protein expression of K2P 2.1 and K2P 6.1 in the endothelium of pulmonary arteries and of K2P 6.1 in bronchial epithelium. PC showed pimozide-sensitive K2P -like K(+) -current activated by docosahexaenoic acid (DHA) in freshly isolated endothelial cells as well as DHA-induced membrane hyperpolarization. Myography on pulmonary arteries showed that DHA induced concentration-dependent instantaneous relaxations that were resistant to endothelial removal and inhibition of NO and prostacyclin synthesis and to a cocktail of blockers of calcium-activated K(+) channels but were abolished by high extracellular (30 mM) K(+) -concentration. Gene expression and protein of K2P 2.1 were not altered in chronic hypoxic mice, while K2P 6.1 was up-regulated by fourfold. In conclusion, the PUFA-activated K2P 2.1 and K2P 6.1 are expressed in murine lung and functional K2P -like channels contribute to endothelium hyperpolarization and pulmonary artery relaxation. The increased K2P 6.1-gene expression may represent a novel counter-regulatory mechanism in pulmonary hypertension and suggest that arterial K2P 2.1 and K2P 6.1 could be novel therapeutic targets.
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