Literature DB >> 17389142

The acid-sensitive potassium channel TASK-1 in rat cardiac muscle.

Caroline Putzke1, Konstantin Wemhöner, Frank B Sachse, Susanne Rinné, Günter Schlichthörl, Xian Tao Li, Lucas Jaé, Ines Eckhardt, Erhard Wischmeyer, Hinnerk Wulf, Regina Preisig-Müller, Jürgen Daut, Niels Decher.   

Abstract

OBJECTIVE: The outward current flowing through the two-pore domain acid-sensitive potassium channel TASK-1 (I(TASK)) and its inhibition via alpha1-adrenergic receptors was studied in rat ventricular cardiomyocytes.
METHODS: Quantitative RT-PCR experiments were carried out with mRNA from rat heart. Patch-clamp recordings were performed in isolated rat cardiomyocytes. TASK-1 and other K+ channels were expressed in Xenopus oocytes to study the pharmacological properties of a new TASK-1 channel blocker, A293.
RESULTS: TASK-1 channels were found to be strongly expressed in rat heart. Analysis of the sensitivity of various K+ channels to A293 in Xenopus oocytes showed that at low concentrations A293 was a selective blocker of TASK-1 channels. I(TASK) in rat cardiomyocytes was dissected by application of A293 and by extracellular acidification to pH 6.0; it had an amplitude of approximately 0.30 pA/pF at +30 mV. Application of 200 nM A293 increased action potential duration (APD(50)) by 31+/-3% at a stimulation rate of 4 Hz. The plausibility of the effects of A293 on APD50 was checked with a mathematical action potential model. Application of the alpha1-adrenergic agonist methoxamine inhibited I(TASK) in Xenopus oocytes co-injected with cRNA for TASK-1 and alpha1A-receptors. In cardiomyocytes, methoxamine inhibited an outward current with characteristics similar to I(TASK). This effect was abolished in the presence of the alpha1A-antagonist 5-methyl-urapidil.
CONCLUSIONS: Our results suggest that in rat cardiomyocytes I(TASK) makes a substantial contribution to the outward current flowing in the plateau range of potentials and that this current component can be inhibited via alpha1A-adrenergic receptors.

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Year:  2007        PMID: 17389142     DOI: 10.1016/j.cardiores.2007.02.025

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  64 in total

1.  TASK1 (K(2P)3.1) K(+) channel inhibition by endothelin-1 is mediated through Rho kinase-dependent phosphorylation.

Authors:  C Seyler; E Duthil-Straub; E Zitron; J Gierten; E P Scholz; R H A Fink; C A Karle; R Becker; H A Katus; D Thomas
Journal:  Br J Pharmacol       Date:  2012-03       Impact factor: 8.739

2.  Breathing Stimulant Compounds Inhibit TASK-3 Potassium Channel Function Likely by Binding at a Common Site in the Channel Pore.

Authors:  Rikki H Chokshi; Aaron T Larsen; Brijesh Bhayana; Joseph F Cotten
Journal:  Mol Pharmacol       Date:  2015-08-12       Impact factor: 4.436

3.  Early remodeling of repolarizing K+ currents in the αMHC403/+ mouse model of familial hypertrophic cardiomyopathy.

Authors:  Rocco Hueneke; Adam Adenwala; Rebecca L Mellor; Jonathan G Seidman; Christine E Seidman; Jeanne M Nerbonne
Journal:  J Mol Cell Cardiol       Date:  2017-01-13       Impact factor: 5.000

4.  Acetylcholine-dependent upregulation of TASK-1 channels in thalamic interneurons by a smooth muscle-like signalling pathway.

Authors:  Michael Leist; Susanne Rinné; Maia Datunashvili; Ania Aissaoui; Hans-Christian Pape; Niels Decher; Sven G Meuth; Thomas Budde
Journal:  J Physiol       Date:  2017-08-03       Impact factor: 5.182

5.  Homeostatic regulation of electrical excitability in physiological cardiac hypertrophy.

Authors:  Kai-Chien Yang; Nicholas C Foeger; Céline Marionneau; Patrick Y Jay; Julie R McMullen; Jeanne M Nerbonne
Journal:  J Physiol       Date:  2010-10-25       Impact factor: 5.182

Review 6.  The CNS under pathophysiologic attack--examining the role of K₂p channels.

Authors:  Petra Ehling; Manuela Cerina; Thomas Budde; Sven G Meuth; Stefan Bittner
Journal:  Pflugers Arch       Date:  2014-12-09       Impact factor: 3.657

7.  Ability to induce atrial fibrillation in the peri-operative period is associated with phosphorylation-dependent inhibition of TWIK protein-related acid-sensitive potassium channel 1 (TASK-1).

Authors:  Erin Harleton; Alessandra Besana; George M Comas; Peter Danilo; Tove S Rosen; Michael Argenziano; Michael R Rosen; Richard B Robinson; Steven J Feinmark
Journal:  J Biol Chem       Date:  2012-12-10       Impact factor: 5.157

8.  Distinct cellular and molecular mechanisms underlie functional remodeling of repolarizing K+ currents with left ventricular hypertrophy.

Authors:  Céline Marionneau; Sylvain Brunet; Thomas P Flagg; Thomas K Pilgram; Sophie Demolombe; Jeanne M Nerbonne
Journal:  Circ Res       Date:  2008-05-01       Impact factor: 17.367

9.  The human cardiac K2P3.1 (TASK-1) potassium leak channel is a molecular target for the class III antiarrhythmic drug amiodarone.

Authors:  Jakob Gierten; Eckhard Ficker; Ramona Bloehs; Patrick A Schweizer; Edgar Zitron; Eberhard Scholz; Christoph Karle; Hugo A Katus; Dierk Thomas
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2009-09-24       Impact factor: 3.000

10.  Novel pharmacological approaches for antiarrhythmic therapy.

Authors:  Ursula Ravens
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2010-01-15       Impact factor: 3.000

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