ArticleThe Journal of physiology2008
Role of sarcolemmal ATP-sensitive K+ channels in the regulation of sinoatrial node automaticity: an evaluation using Kir6.2-deficient mice.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Potential roles of β3-adrenergic receptor in heart rate regulation via sinus node activity and local adipocyte metabolism.The journal of physiological sciences : JPS · 2026Article
- Pacemaker Channels and the Chronotropic Response in Health and Disease.Circulation research · 2024Review
- Kir6.1 and SUR2B in Cantú syndrome.American journal of physiology. Cell physiology · 2022Review
- Cardiac dysfunction in spontaneously hypertensive old rats is associated with a significant decrease of SUR2 expression.Molecular and cellular biochemistry · 2021Article
- Amorphous SiO2 nanoparticles promote cardiac dysfunction via the opening of the mitochondrial permeability transition pore in rat heart and human cardiomyocytes.Particle and fibre toxicology · 2020Article
- ATP-sensitive potassium channels in the sinoatrial node contribute to heart rate control and adaptation to hypoxia.The Journal of biological chemistry · 2018Article
- Potassium channels in the sinoatrial node and their role in heart rate control.Channels (Austin, Tex.) · 2018Review
- Adenosine Triphosphate-Sensitive Potassium Currents in Heart Disease and Cardioprotection.Cardiac electrophysiology clinics · 2016Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Functional roles of KATP channel subunits in metabolic inhibition.Journal of molecular and cellular cardiology · 2013Article
- KATP channels and cardiovascular disease: suddenly a syndrome.Circulation research · 2013Review
- Ca²+/calmodulin-dependent protein kinase II (CaMKII) activity and sinoatrial nodal pacemaker cell energetics.PloS one · 2013Article
- Distinct localization and modulation of Cav1.2 and Cav1.3 L-type Ca2+ channels in mouse sinoatrial node.The Journal of physiology · 2012Article
- Role of KATP channel in electrical depression and asystole during long-duration ventricular fibrillation in ex vivo canine heart.American journal of physiology. Heart and circulatory physiology · 2012Article
- A mathematical model of action potentials of mouse sinoatrial node cells with molecular bases.American journal of physiology. Heart and circulatory physiology · 2011Article
- Muscle KATP channels: recent insights to energy sensing and myoprotection.Physiological reviews · 2010Review
- Differential K(ATP) channel pharmacology in intact mouse heart.Journal of molecular and cellular cardiology · 2010Article
- KATP channel Kir6.2 E23K variant overrepresented in human heart failure is associated with impaired exercise stress response.Human genetics · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of cardiac sarcolemmal ATP-sensitive K+ (K(ATP)) channels in the regulation of sinoatrial node (SAN) automaticity is not well defined. Using mice with homozygous knockout (KO) of the Kir6.2 (a pore-forming subunit of cardiac K(ATP) channel) gene, we investigated the pathophysiological role of K(ATP) channels in SAN cells during hypoxia. Langendorff-perfused mouse hearts were exposed to hypoxic and glucose-free conditions (hypoxia). After 5 min of hypoxia, sinus cycle length (CL) was prolonged from 207 +/- 10 to 613 +/- 84 ms (P < 0.001) in wild-type (WT) hearts. In Kir6.2 KO hearts, CL was slightly prolonged from 198 +/- 17 to 265 +/- 32 ms. The CL of spontaneous action potentials of WT SAN cells, recorded in the current-clamp mode, was markedly prolonged from 410 +/- 56 to 605 +/- 108 ms (n = 6, P < 0.05) with a decrease of the slope of the diastolic depolarization (SDD) after the application of the K+ channel opener pinacidil (100 microm). Pinacidil induced a glibenclamide (1 microm)-sensitive outward current, which was recorded in the voltage-clamp mode, only in WT SAN cells. During metabolic inhibition by 2,4-dinitrophenol, CL was prolonged from 292 +/- 38 to 585 +/- 91 ms (P < 0.05) with a decrease of SDD in WT SAN cells but not in Kir6.2 KO SAN cells. Diastolic Ca2+ concentration, measured by fluo-3 fluorescence, was decreased in WT SAN cells but increased in Kir6.2 KO SAN cells after short-term metabolic inhibition. In conclusion, the present study using Kir6.2 KO mice indicates that, during hypoxia, activation of sarcolemmal K(ATP) channels in SAN cells inhibits SAN automaticity, which is important for the protection of SAN cells.
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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.