Comparative Effects of Glibenclamide, Tedisamil, Dofetilide, E-4031, and BRL-32872 on Protein Kinase A-Activated Chloride Current in Guinea Pig Ventricular Myocytes

1998 ◽  
Vol 31 (4) ◽  
pp. 551-557 ◽  
Author(s):  
Jean-François Faivre ◽  
Sabine Rouanet ◽  
Antoine Bril
2001 ◽  
Vol 441 (6) ◽  
pp. 807-815 ◽  
Author(s):  
Jens Kockskämper ◽  
Kirsty Sendhoff ◽  
Simone Erlenkamp ◽  
Frank Bordusa ◽  
Vaclav Cerovsky ◽  
...  

2000 ◽  
Vol 279 (5) ◽  
pp. H2104-H2115 ◽  
Author(s):  
Jiequan Zhu ◽  
Gregory R. Ferrier

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.


1999 ◽  
Vol 438 (2) ◽  
pp. 205-212 ◽  
Author(s):  
D. B. Duridanova ◽  
P. S. Petkova-Kirova ◽  
L. T. Lubomirov ◽  
H. Gagov ◽  
K. Boev

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