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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
Published on: July 16, 2013
Modulation of myocardial activity by extracellular ATP
G Vassort1, M Pucéat, F Scamps
1INSERM U-390 Physiopathologie Cardiovasculaire, CHU Arnaud de Villejeuve, F-34295 Montpellier, France.
Trends in Cardiovascular Medicine
|January 20, 2011
Summary
Extracellular adenosine triphosphate (ATP) affects cardiac cells by increasing calcium currents and contractility via P2 purinoceptor stimulation. Rapid ATP application can cause arrhythmias due to membrane depolarization and cell acidification.
Area of Science:
- Cardiology
- Cell Physiology
- Biochemistry
Background:
- Extracellular adenosine triphosphate (ATP) plays a crucial role in cellular signaling.
- Cardiac cells possess P2 purinoceptors that respond to extracellular ATP.
- Dysregulation of extracellular ATP can impact cardiac function.
Purpose of the Study:
- To investigate the functional changes induced by extracellular ATP in cardiac cells.
- To elucidate the mechanisms underlying ATP-induced cardiac cell responses.
- To assess the potential role of ATP in cardiac arrhythmias.
Main Methods:
- Micromolar concentration stimulation of cardiac cells with extracellular ATP.
- Measurement of calcium currents.
- Assessment of membrane potential and intracellular pH changes.
- Investigation of ion channel and exchanger activity.
Main Results:
- Extracellular ATP stimulation led to an increase in Ca current and a positive inotropic effect.
- Rapid ATP application caused membrane depolarization via activation of Cl conductance.
- ATP induced cellular acidification through stimulation of the Cl-HCO3 exchanger.
- These changes suggest a link between ATP release and cardiac arrhythmias.
Conclusions:
- Extracellular ATP at micromolar concentrations significantly alters cardiac cell function.
- P2 purinoceptor activation mediates key electrophysiological and mechanical responses.
- ATP-induced depolarization and acidification are potential mechanisms contributing to cardiac arrhythmias under pathophysiological conditions.
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