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Enhanced Late I Na Induces Intracellular Ion Disturbances and Automatic Activity in the Guinea Pig Pulmonary Vein Cardiomyocytes
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Enhanced Late I Na Induces Intracellular Ion Disturbances and Automatic Activity in the Guinea Pig Pulmonary Vein Cardiomyocytes
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Journal Article
Enhanced Late I Na Induces Intracellular Ion Disturbances and Automatic Activity in the Guinea Pig Pulmonary Vein Cardiomyocytes
2024
Overview
The effects of enhanced late I
, a persistent component of the Na
channel current, on the intracellular ion dynamics and the automaticity of the pulmonary vein cardiomyocytes were studied with fluorescent microscopy. Anemonia viridis toxin II (ATX- II), an enhancer of late I
, caused increases in the basal Na
and Ca
concentrations, increases in the number of Ca
sparks and Ca
waves, and the generation of repetitive Ca
transients. These phenomena were inhibited by eleclazine, a blocker of the late I
; SEA0400, an inhibitor of the Na
/Ca
exchanger (NCX); H89, a protein kinase A (PKA) inhibitor; and KN-93, a Ca
/calmodulin-dependent protein kinase II (CaMKII) inhibitor. These results suggest that enhancement of late I
in the pulmonary vein cardiomyocytes causes disturbance of the intracellular ion environment through activation of the NCX and Ca
-dependent enzymes. Such mechanisms are probably involved in the ectopic electrical activity of the pulmonary vein myocardium.
Subject
Action Potentials - drug effects
/ Aniline Compounds - pharmacology
/ Animals
/ Calcium Signaling - drug effects
/ Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism
/ Cnidarian Venoms - pharmacology
/ Cyclic AMP-Dependent Protein Kinases - metabolism
/ Male
/ Myocytes, Cardiac - drug effects
/ Myocytes, Cardiac - metabolism
/ Pulmonary Veins - drug effects
/ Pulmonary Veins - metabolism
/ Sodium Channels - metabolism
