Stimulation of Na/Ca exchange by the β-adrenergic/protein kinase A pathway in guinea-pig ventricular myocytes at 37°C

2000 ◽  
Vol 439 (6) ◽  
pp. 822-828 ◽  
Author(s):  
L. Perchenet ◽  
A.K. Hinde ◽  
K.C.R. Patel ◽  
J.C. Hancox ◽  
A.J. Levi
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Protein Kinase A ◽  
Ventricular Myocytes ◽  
Kinase A ◽  
Stimulation Of

Differences in the protein-kinase-A-dependent regulation of CFTR Cl - channels and Na + -K + pumps in guinea-pig ventricular myocytes

2001 ◽  
Vol 441 (6) ◽  
pp. 807-815 ◽  
Author(s):  
Jens Kockskämper ◽  
Kirsty Sendhoff ◽  
Simone Erlenkamp ◽  
Frank Bordusa ◽  
Vaclav Cerovsky ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Protein Kinase A ◽  
Ventricular Myocytes ◽  
Cl Channels ◽  
Kinase A

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

2000 ◽  
Vol 279 (5) ◽  
pp. H2104-H2115 ◽  
Author(s):  
Jiequan Zhu ◽  
Gregory R. Ferrier
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Protein Kinase A ◽  
Cardiac Myocytes ◽  
High Resistance ◽  
Ventricular Myocytes ◽  
Release Mechanism ◽  
Pipette Solution ◽  
Kinase A ◽  
Caffeine Contractures

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.

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