ArticleHypertension (Dallas, Tex. : 1979)2011
Disruption of K(2P)6.1 produces vascular dysfunction and hypertension in mice.
Article in Hypertension (Dallas, Tex. : 1979), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Structural evidence that a lipid plug controls KNature communications · 2026Article
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- Structure-Function Relationships of KAdvances in experimental medicine and biology · 2026Review
- K2P channels as emerging therapeutic targets for pain: insights from functional studies and transcriptomic analyses.Frontiers in pharmacology · 2026Review
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- Research progress of two-pore potassium channel in myocardial ischemia-reperfusion injury.Frontiers in physiology · 2024Review
- Endosomal trafficking of two-pore KeLife · 2023Article
- Two-Pore-Domain Potassium (KCells · 2021Review
- Restructuring the Gut Microbiota by Intermittent Fasting Lowers Blood Pressure.Circulation research · 2021Article
- Lipid-protein forces predict conformational changes in a mechanosensitive channel.European biophysics journal : EBJ · 2021Article
- Current Drug Treatment Strategies for Atrial Fibrillation and TASK-1 Inhibition as an Emerging Novel Therapy Option.Frontiers in pharmacology · 2021Review
- Potassium Channel Protein KCNK6 Promotes Breast Cancer Cell Proliferation, Invasion, and Migration.Frontiers in cell and developmental biology · 2021Article
- Review
- Pharmacologic TWIK-Related Acid-Sensitive K+ Channel (TASK-1) Potassium Channel Inhibitor A293 Facilitates Acute Cardioversion of Paroxysmal Atrial Fibrillation in a Porcine Large Animal Model.Journal of the American Heart Association · 2020Article
- Distinct Molecular Mechanisms Underlying Potassium Efflux for NLRP3 Inflammasome Activation.Frontiers in immunology · 2020Review
- The Experimental TASK-1 Potassium Channel Inhibitor A293 Can Be Employed for Rhythm Control of Persistent Atrial Fibrillation in a Translational Large Animal Model.Frontiers in physiology · 2020Article
- Twik-2Physiological reports · 2019Article
- The TWIK2 Potassium Efflux Channel in Macrophages Mediates NLRP3 Inflammasome-Induced Inflammation.Immunity · 2018Article
- Microglial Ramification, Surveillance, and Interleukin-1β Release Are Regulated by the Two-Pore Domain KNeuron · 2018Article
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8 authors at 1 institution in 1 country.
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Abstract
K(2P)6.1, a member of the 2-pore domain K channel family, is highly expressed in the vascular system; however, its function is unknown. We tested the following hypotheses. K(2P)6.1 regulates the following: (1) systemic blood pressure; (2) the contractile state of arteries; (3) vascular smooth muscle cell migration; (4) proliferation; and/or (5) volume regulation. Mice lacking K(2P)6.1 (KO) were generated by deleting exon 1 of Kcnk6. Mean arterial blood pressure in both anesthetized and awake KO mice was increased by 17±2 and 26±3 mm Hg, respectively (P<0.05). The resting membrane potential in freshly dispersed vascular smooth muscle cells was depolarized by 17±2 mV in the KO compared with wild-type littermates (P<0.05). The contractile responses to KCl (P<0.05) and BAY K 8644 (P<0.01), an activator of L-type calcium channels, were enhanced in isolated segments of aorta from KO mice. However, there was no difference in the current density of L-type calcium channels. Responses to U46619, an agent that activates rho kinase, showed an enhanced contraction in aorta from KO mice (P<0.001). The BAY K 8644-mediated increase in contraction was decreased to wild-type levels when treated with Y27632, a rho kinase inhibitor, (P<0.05). K(2P)6.1 does not appear to be involved with migration, proliferation, or volume regulation in cultured vascular smooth muscle cells. We conclude that K(2P)6.1 deficiency induces vascular dysfunction and hypertension through a mechanism that may involve smooth muscle cell depolarization and enhanced rho kinase activity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.