ArticleDiabetologia2008
Thiazolidinedione drugs block cardiac KATP channels and may increase propensity for ischaemic ventricular fibrillation in pigs.
Article in Diabetologia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- Integrating Transcriptomic and Targeted New Approach Methodologies into a Tiered Framework for Chemical Bioactivity Screening.Environmental health perspectives · 2025Article
- Rosiglitazone Does Not Show Major Hidden Cardiotoxicity in Models of Ischemia/Reperfusion but Abolishes Ischemic Preconditioning-Induced Antiarrhythmic Effects in Rats In Vivo.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Structural and Electrical Remodeling of the Sinoatrial Node in Diabetes: New Dimensions and Perspectives.Frontiers in endocrinology · 2022Review
- The forgotten type 2 diabetes mellitus medicine: rosiglitazone.Diabetology international · 2022Review
- Computational Identification of Novel Kir6 Channel Inhibitors.Frontiers in pharmacology · 2019Article
- Ventricular Arrhythmias in First Acute Myocardial Infarction: Epidemiology, Mechanisms, and Interventions in Large Animal Models.Frontiers in cardiovascular medicine · 2019Review
- Metformin prevents ischaemic ventricular fibrillation in metabolically normal pigs.Diabetologia · 2017Article
- PPARPPAR research · 2017Review
- Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel.The journal of physiological sciences : JPS · 2014Article
- Minireview: Challenges and opportunities in development of PPAR agonists.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Chemical proteomics-based analysis of off-target binding profiles for rosiglitazone and pioglitazone: clues for assessing potential for cardiotoxicity.Journal of medicinal chemistry · 2012Article
- PPAR-γ as a therapeutic target in cardiovascular disease: evidence and uncertainty.Journal of lipid research · 2012Review
- Rosiglitazone selectively inhibits K(ATP) channels by acting on the K(IR) 6 subunit.British journal of pharmacology · 2012Article
- Thiazolidinedione drugs promote onset, alter characteristics, and increase mortality of ischemic ventricular fibrillation in pigs.Cardiovascular drugs and therapy · 2012Article
- Rosiglitazone inhibits vascular KATP channels and coronary vasodilation produced by isoprenaline.British journal of pharmacology · 2011Article
- Rosiglitazone inhibits Kv4.3 potassium channels by open-channel block and acceleration of closed-state inactivation.British journal of pharmacology · 2011Article
- Cardiac ion channel modulation by the hypoglycaemic agent rosiglitazone.British journal of pharmacology · 2011Article
- Effects of rosiglitazone on the configuration of action potentials and ion currents in canine ventricular cells.British journal of pharmacology · 2011Article
- PPARγ activator, rosiglitazone: Is it beneficial or harmful to the cardiovascular system?World journal of cardiology · 2011Article
- Can the electrophysiological action of rosiglitazone explain its cardiac side effects?Current medicinal chemistry · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisOpening of ATP-sensitive potassium (K(ATP)) channels during myocardial ischaemia shortens action potential duration and is believed to be an adaptive, energy-sparing response. Thiazolidinedione drugs block K(ATP) channels in non-cardiac cells in vitro. This study determined whether thiazolidinedione drugs block cardiac K(ATP) channels in vivo.
methodsExperiments in 68 anaesthetised pigs determined: (1) effects of inert vehicle, troglitazone (10 mg/kg i.v.) or rosiglitazone (0.1 or 1.0 mg/kg i.v.) on epicardial monophasic action potential (MAP) during 90 min low-flow ischaemia; (2) effects of troglitazone, rosiglitazone or pioglitazone (1 mg/kg i.v.) on response of MAP to intracoronary infusion of a K(ATP) channel opener, levcromakalim; and (3) effects of inert vehicle, rosiglitazone (1 mg/kg i.v.) or the sarcolemmal K(ATP) blocker HMR-1098 on time to onset of ventricular fibrillation following complete coronary occlusion.
resultsWith vehicle, epicardial MAP shortened by 44+/-9 ms during ischaemia. This effect was attenuated to 12+/-8 ms with troglitazone and 6+/-6 ms with rosiglitazone (p<0.01 for both vs vehicle), suggesting K(ATP) blockade. Intracoronary levcromakalim shortened MAP by 38+/-10 ms, an effect attenuated to 12+/-8, 13+/-4 and 9+/-5 ms during co-treatment with troglitazone, rosiglitazone or pioglitazone (p<0.05 for each), confirming K(ATP) blockade. During coronary occlusion, median time to ventricular fibrillation was 29 min in pigs treated with vehicle and 6 min in pigs treated with rosiglitazone or HMR-1098 (p<0.05 for both vs vehicle), indicating that K(ATP) blockade promotes ischaemic ventricular fibrillation in this model. CONCLUSIONS/
interpretationThiazolidinedione drugs block cardiac K(ATP) channels at clinically relevant doses and promote onset of ventricular fibrillation during severe ischaemia.
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Registered trials
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