Key result
The voltage-sensitive release mechanism in guinea pig ventricular myocytes is facilitated by CamK and PKA, with combined inhibition by KN-62 and H-89 reducing VSRM contractions by 93%.
Population
Guinea pig ventricular myocytes
Comparison
Dialysis with 2-5 microM calmodulin, and… vs Standard pipette solution without calmodulin
Design
Preclinical
Authors
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Should not alter clinical practice; hypothesis-generating for human VSRM regulation and Ca2+ handling.
The voltage-sensitive release mechanism in cardiac myocytes is facilitated by both Ca2+-calmodulin-dependent kinase and protein kinase A pathways.
Zhu et al. (2000) studied this question. Calmodulin and kinase inhibitors (KN-62, H-89) vs. Standard pipette solution was evaluated on VSRM contractions and Ca2+ transients. The voltage-sensitive release mechanism in guinea pig ventricular myocytes is facilitated by CamK and PKA, with combined inhibition by KN-62 and H-89 reducing VSRM contractions by 93%.
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