The role of reduced potassium conductance in generating triggered activity in guinea-pig ventricular muscle

• Published in: Journal of molecular and cellular cardiology Vol. 22; no. 5; pp. 619 - 628
• Main Authors: Gilat, Eran, Nordin, Charles W., Aronson, Ronald S.
• Format: Journal Article
• Language: English
• Published: Kent Elsevier Ltd 01.05.1990; Elsevier
• Subjects: Animals; Biological and medical sciences; Biological Transport - drug effects; Biological Transport - physiology; Cell Membrane - drug effects; Cell Membrane - physiology; Cell Membrane - ultrastructure; Delayed afterdepolarizations; Electric Conductivity - drug effects; Electric Conductivity - physiology; Fundamental and applied biological sciences. Psychology; Guinea Pigs; Heart; Heart Ventricles - metabolism; Heart Ventricles - ultrastructure; Male; Membrane conductance; Membrane Potentials - drug effects; Membrane Potentials - physiology; Ouabain - pharmacology; Papillary Muscles - metabolism; Papillary Muscles - physiology; Papillary Muscles - ultrastructure; Potassium - metabolism; Potassium - pharmacokinetics; Potassium - physiology; Potassium Channels - drug effects; Potassium Channels - physiology; Potassium Channels - ultrastructure; Potassium conductance; Tetraethylammonium; Tetraethylammonium Compounds - pharmacology; Triggered activity; Ventricular Function; Ventricular muscle; Vertebrates: cardiovascular system; Delayed afterdepolarizations; Membrane conductance; Ventricular muscle; Potassium conductance; Triggered activity; Heart; Depolarization; Vertebrata; Mammalia; Guinea pig; Induction; Rodentia; Electrophysiology; Electrical conductance; Heart ventricle; Potassium; Biological activity
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1016/0022-2828(90)90963-3

This study investigates the role of reducing potassium conductance ( g K ) in generating delayed afterdepolarizations and triggered activity in small preparations of ventricular muscle from guinea-pig hearts. We used agents believed to reduce g K (low or absent K 0, tetraethylammonium (TEA), CsCl) and we used ouabain (10 −6 m) to induce delayed afterdepolarizations. Treatment with ouabain only caused subthreshold delayed afterdepolarizations or occasionally non-sustained triggered activity. Exposure to Tyrode's solution with K reduced from 4 to 2 m m or K-free Tyrode's solution, with or without ouabain, caused subthreshold delayed afterdepolarizations and sometimes non-sustained triggered activity. Exposure to Tyrode's solution containing TEA and ouabain caused sustained triggered activity, supporting the hypothesis that accumulation of extracellular K inhibits the development of triggered activity. Presumably, the reduction in g K caused by TEA is not reversed by accumulation of extracellular K so that the delayed afterdepolarizations in the presence of persistently reduced g K are large enough to induced sustained triggered activity. Under extreme conditions, when Cs replaced K and half the NaCl was replaced by TEA, delayed afterdepolarizations occurred in the presence of markedly reduced g K , the result being the rapid development of sustained triggered activity, even at the basic drive rate of 1 Hz. Our results suggest that reduced g K plays an important role in the development of triggered activity.