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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Intracellular Cs⁺ activates the PKA pathway, revealing a fast, reversible, Ca²⁺-dependent inactivation of L-type Ca²⁺ current

Centre National de la Recherche Scientifique Unité Mixte de Recherche 6542, Faculté des Sciences, Université de Tours, 37041 Tours Cedex, France

Submitted 13 August 2002 ; accepted in final form 26 March 2003

Inactivation of the L-type Ca²⁺ current (I_CaL) was studied in isolated guinea pig ventricular myocytes with different ionic solutions. Under basal conditions, I_CaL of 82% of cells infused with Cs⁺-based intracellular solutions showed enhanced amplitude with multiphasic decay and diastolic depolarization-induced facilitation. The characteristics of I_CaL in this population of cells were not due to contamination by other currents or an artifact. These phenomena were reduced by ryanodine, caffeine, cyclopiazonic acid, the protein kinase A inhibitor H-89, and the cAMP-dependent protein kinase inhibitor. Forskolin and isoproterenol increased I_CaL by only 60% in these cells. Cells infused with either N-methyl-D-glucamine or K⁺-based intracellular solutions did not show multiphasic decay or facilitation under basal conditions. Isoproterenol increased I_CaL by 200% in these cells. In conclusion, we show that multiphasic inactivation of I_CaL is due to Ca²⁺-dependent inactivation that is reversible on a time scale of tens of milliseconds. Cs⁺ seems to activate the cAMP-dependent protein kinase pathway when used as a substitute for K⁺ in the pipette solution.

L-type calcium current; calcium-dependent inactivation; facilitation; phosphorylation; cesium

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