AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 279: H2104-H2115, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2104-H2115, November 2000

Regulation of a voltage-sensitive release mechanism by Ca2+-calmodulin-dependent kinase in cardiac myocytes

Jiequan Zhu and Gregory R. Ferrier

Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7

A role for Ca2+-calmodulin-dependent kinase (CamK) in regulation of the voltage-sensitive release mechanism (VSRM) was investigated in guinea pig ventricular myocytes. Voltage clamp was used to separate the VSRM from Ca2+-induced Ca2+ release (CICR). VSRM contractions and Ca2+ transients were absent in cells dialyzed with standard pipette solution but present when 2-5 µM calmodulin was included. Effects of calmodulin were blocked by KN-62 (CamK inhibitor), but not H-89, a protein kinase A (PKA) inhibitor. Ca2+ current and caffeine contractures were not affected by calmodulin. Transient-voltage relations were bell-shaped without calmodulin, but they were sigmoidal and typical of the VSRM with calmodulin. Contractions with calmodulin exhibited inactivation typical of the VSRM. These contractions were inhibited by rapid application of 200 µM of tetracaine, but not 100 µM of Cd2+, whereas CICR was inhibited by Cd2+ but not tetracaine. In undialyzed myocytes (high-resistance microelectrodes), KN-62 or H-89 each reduced amplitudes of VSRM contractions by ~50%, but together they decreased VSRM contractions by 93%. Thus VSRM is facilitated by CamK or PKA, and both pathways regulate the VSRM in undialyzed cells.

excitation-contraction coupling; cardiac muscle; protein kinase


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