TY - JOUR
T1 - The role of reduced potassium conductance in generating triggered activity in guinea-pig ventricular muscle
AU - Gilat, Eran
AU - Nordin, Charles W.
AU - Aronson, Ronald S.
N1 - Funding Information:
Acknowledgements We gratefully acknowledge the careful preparation of the manuscript by JoAnne Pawlowski. This work was supported by NIH grant HL 32688.
PY - 1990/5
Y1 - 1990/5
N2 - This study investigates the role of reducing potassium conductance (gK) in generating delayed afterdepolarizations and triggered activity in small preparations of ventricular muscle from guinea-pig hearts. We used agents believed to reduce gK (low or absent K0, 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 mm 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 gK caused by TEA is not reversed by accumulation of extracellular K so that the delayed afterdepolarizations in the presence of persistently reduced gK 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 gK, the result being the rapid development of sustained triggered activity, even at the basic drive rate of 1 Hz. Our results suggest that reduced gK plays an important role in the development of triggered activity.
AB - This study investigates the role of reducing potassium conductance (gK) in generating delayed afterdepolarizations and triggered activity in small preparations of ventricular muscle from guinea-pig hearts. We used agents believed to reduce gK (low or absent K0, 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 mm 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 gK caused by TEA is not reversed by accumulation of extracellular K so that the delayed afterdepolarizations in the presence of persistently reduced gK 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 gK, the result being the rapid development of sustained triggered activity, even at the basic drive rate of 1 Hz. Our results suggest that reduced gK plays an important role in the development of triggered activity.
KW - Delayed afterdepolarizations
KW - Membrane conductance
KW - Potassium conductance
KW - Triggered activity
KW - Ventricular muscle
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U2 - 10.1016/0022-2828(90)90963-3
DO - 10.1016/0022-2828(90)90963-3
M3 - Article
C2 - 2388285
AN - SCOPUS:0025367432
SN - 0022-2828
VL - 22
SP - 619
EP - 628
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
IS - 5
ER -