Caffeine-induced decreases in the inward rectifier potassium and the inward calcium currents in rat ventricular myocytes.
The effects of high (20 mM) concentrations of caffeine were studied on the transmembrane voltage and currents in rat single ventricular myocytes by the whole cell configuration of the patch clamp technique. Rapid application of caffeine released Ca2+ from the sarcoplasmic reticulum and induced a Ni(2+)-sensitive transient inward current with concomitant change of the transmembrane voltage from -72.6 +/- 0.4 to -68.0 +/- 0.6 mV (n = 4). Maintained application of caffeine lengthened the action potential duration (APD90) from 66.7 +/- 16.9 to 135.1 +/- 34.1 ms (n = 4) and depressed the amplitude of both the inward rectifier potassium and the inward calcium currents. It is concluded that these effects of caffeine should be recognized when it is used as a tool to study electromechanical coupling.
Varro
A
A
Department of Pharmacology, Albert Szent-Györgyi Medical University, Szeged, Hungary.
Hester
S
S
Papp
J G
JG
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002110:Caffeine / Q000494:pharmacology*; D015220:Calcium Channels / Q000187:drug effects*; D006321:Heart / Q000187:drug effects; D006352:Heart Ventricles / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D066298:In Vitro Techniques; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects*; D051381:Rats; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism
D015220:Calcium Channels; D015221:Potassium Channels; D002110:Caffeine