The study identifies a differential distribution of persistent sodium current across the ventricular wall, which computer modeling suggests contributes to the dispersion of action potential duration.
Reduced midmyocardial I(pNa) may drive APD dispersion; leaves open role in arrhythmogenesis.
A tetrodotoxin-sensitive persistent sodium current, I(pNa), was found in guinea pig ventricular myocytes by whole-cell patch clamping. This current was characterized in cells derived from the basal left ventricular subendocardium, midmyocardium, and subepicardium. Midmyocardial cells show a statistically significant (P<0.05) smaller I(pNa) than subendocardial and subepicardial myocytes. There was no significant difference in I(pNa) current density between subepicardial and subendocardial cells. Computer modeling studies support a role of this current in the dispersion of action potential duration across the ventricular wall.
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Sakmann et al. (2000) studied this question.
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