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Gadolinium blocks the delayed rectifier potassium current in isolated guinea‐pig ventricular myocytes
Author(s) -
Hongo K,
Pascarel C,
Cazorla O,
Gannier F,
Le Guennec JY,
White E
Publication year - 1997
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1997.sp004053
Subject(s) - nifedipine , inward rectifier potassium ion channel , biophysics , patch clamp , chemistry , myocyte , guinea pig , depolarization , electrophysiology , blockade , medicine , voltage clamp , potassium , endocrinology , calcium , ion channel , biology , biochemistry , receptor , organic chemistry
The effect of Gd3+ on the delayed rectifier potassium current (IK) in single guinea‐pig ventricular myocytes was tested using whole‐cell patch‐clamp techniques. It was found that Gd3+ blocked 70% of the IK tail current at a concentration of 100 microM. The EC50 was 24 microM. Action potential durations were, however, reduced, consistent with a predominant effect on depolarizing L‐type Ca2+ current (Ica.L). In the presence of 5 microM nifedipine Gd3+ prolonged the action potential. Using carbon fibres to stretch cells we observed that 10 microM Gd3+ was not effective in reducing a large stretch‐activated increase in resting calcium. Modelling studies using the OXSOFT HEART program suggest that this lack of response is influenced by blockade of repolarizing current but is best reproduced by additional blockade of Ca2+ extrusion via the Na(+)ࢤCa2+ exchanger. When Gd3+ is used as a blocker of stretch‐activated channels its actions upon both Ica.L and IK must therefore be accounted for.