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Am J Physiol Cell Physiol (April 9, 2003). doi:10.1152/ajpcell.00368.2002
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Submitted on August 13, 2002
Accepted on March 26, 2003

INTRACELLULAR CAESIUM ACTIVATES THE PKA PATHWAY REVEALING A FAST REVERSIBLE CALCIUM DEPENDENT INACTIVATION OF L-TYPE CALCIUM CURRENT

Fabien Brette1*, Alain Lacampagne2, Laurent Salle3, Ian Findlay4, and Jean-Yves Le Guennec5

1 School of Biomedical Sciences, University of Leeds, Leeds, United Kingdom
2 Physiopathologie Cardiovasculaire, INSERM U390, Montpellier, France
3 Laboratoire de Physiologie Cellulaire, Universite de Caen, Caen, France
4 CNRS UMR 6542, Universite de Tours, Tours, France
5 CNRS UMR 6542, Universite de Tours, Tours, France; INSERM Emi 0211, Universite de Tours, Tours, France

* To whom correspondence should be addressed. E-mail: bmsfpb{at}bms.leeds.ac.uk.

Inactivation of the L-type Ca2+ current (ICaL) was studied in isolated guinea-pig ventricular myocytes with different ionic solutions. Under basal conditions, ICaL of 82% of cells infused with Cs+-based intracellular solutions showed enhanced amplitude with multiphasic decay and diastolic depolarization induced facilitation. The characteristics of ICaL in this population of cells were not due to contamination by other currents nor an artifact. These phenomena were reduced by ryanodine, caffeine, cyclopiazonic acid, the protein kinase A inhibitor H-89 and PKI. Forskolin and isoproterenol increased ICaL by only ~60% in these cells. Cells infused with either NMDG or K+ based intracellular solutions did not show multiphasic decay or facilitation under basal conditions. Isoproterenol increased ICaL by ~200% in these cells. In conclusion, we show that multiphasic inactivation of ICaL is due to Ca2+-dependent inactivation which is reversible on a time scale of 10's of ms. Cs+ seems to activate the PKA pathway when used as a substitute for K+ in the pipette solution.




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