ArticleBritish journal of pharmacology2000
Inhibitory effects of JTV-519, a novel cardioprotective drug, on potassium currents and experimental atrial fibrillation in guinea-pig hearts.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 55 citations in OpenAlex.
- Pharmacological study of the safety, efficacy, and potential of M201-A on paroxysmal and persistent atrial fibrillation.The Journal of pharmacology and experimental therapeutics · 2025Trial
- Crosstalk between Ryanodine Receptor 2 Dysfunction and FK506-Binding Proteins in Pulmonary Hypertension.Cardiovascular drugs and therapy · 2026Review
- Role of ryanodine receptor 2 and FK506-binding protein 12.6 dissociation in pulmonary hypertension.The Journal of general physiology · 2023Article
- Differential Modulation ofFrontiers in physiology · 2019Article
- Calcium-mediated cellular triggered activity in atrial fibrillation.The Journal of physiology · 2017Review
- Calcium Signaling and Cardiac Arrhythmias.Circulation research · 2017Review
- New antiarrhythmic targets to control intracellular calcium handling.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
- The ryanodine receptor leak: how a tattered receptor plunges the failing heart into crisis.Heart failure reviews · 2013Review
- Cardiac ryanodine receptor in metabolic syndrome: is JTV519 (K201) future therapy?Diabetes, metabolic syndrome and obesity : targets and therapy · 2012Article
- Mechanisms of termination and prevention of atrial fibrillation by drug therapy.Pharmacology & therapeutics · 2011Review
- Targeting ryanodine receptors for anti-arrhythmic therapy.Acta pharmacologica Sinica · 2011Review
- The ryanodine receptor channel as a molecular motif in atrial fibrillation: pathophysiological and therapeutic implications.Cardiovascular research · 2011Review
- Atrial Ca2+ signaling in atrial fibrillation as an antiarrhythmic drug target.Naunyn-Schmiedeberg's archives of pharmacology · 2010Review
- Calmodulin kinase II, sarcoplasmic reticulum Ca2+ leak, and atrial fibrillation.Trends in cardiovascular medicine · 2010Review
- Pharmacological characteristics and clinical applications of K201.Current clinical pharmacology · 2009Review
- Effect of K201, a novel antiarrhythmic drug on calcium handling and arrhythmogenic activity of pulmonary vein cardiomyocytes.British journal of pharmacology · 2008Article
- 2APB- and JTV519(K201)-sensitive micro Ca2+ waves in arrhythmogenic Purkinje cells that survive in infarcted canine heart.Heart rhythm · 2004Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We investigated the effects of JTV-519 (4-[3-(4-benzylpiperidin-1-yl)propionyl]-7-methoxy-2,3,4, 5-tetrahydro-1,4-benzothiazepine monohydrochloride), a novel cardioprotective drug, on the repolarizing K(+) currents in guinea-pig atrial cells by use of patch-clamp techniques. We also evaluated the effects of JTV-519 on experimental atrial fibrillation (AF) in isolated guinea-pig hearts. 2. In atrial cells stimulated at 0.2 Hz, JTV-519 in concentrations of 0.3 and 1 microM slightly prolonged the action potential duration (APD). The drug also reversed the action potential shortening induced by the muscarinic agonist carbachol in a concentration-dependent manner. 3. The muscarinic acetylcholine receptor-operated K(+) current (I(K.ACh)) was activated by the extracellular application of carbachol (1 microM), adenosine (10 microM) or by the intracellular loading of GTP gamma S (100 microM). JTV-519 inhibited the carbachol-, adenosine- and GTP gamma S-induced I(K.ACh) with the IC(50) values of 0.12, 2.29 and 2.42 microM, respectively, suggesting that the drug may inhibit I(K.ACh) mainly by blocking the muscarinic receptors. 4. JTV-519 (1 microM) inhibited the delayed rectifier K(+) current (I(K)). Electrophysiological analyses indicated that the drug preferentially inhibits I(Kr) (rapidly activating component) but not I(Ks) (slowly activating component). 5. In isolated hearts, perfusion of carbachol (1 microM) shortened monophasic action potential (MAP) and effective refractory period (ERP), and lowered atrial fibrillation threshold (AFT). Addition of JTV-519 (1 microM) inhibited the induction of AF by prolonging MAP and ERP. 6. We conclude that JTV-519 can exert antiarrhythmic effects against AF by inhibiting repolarizing K(+) currents. The drug may be useful for the treatment of AF in patients with ischaemic heart disease.
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