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• W2065355000 endingPage "2552" @default.
• W2065355000 startingPage "2545" @default.
• W2065355000 abstract "Background —Alterations in K + channel expression and gating are thought to be the major cause of action potential remodeling in heart failure (HF). We previously reported the existence of a late Na + current (I NaL ) in cardiomyocytes of dogs with chronic HF, which suggested the importance of the Na + channel in this remodeling process. The present study examined whether this I NaL exists in cardiomyocytes isolated from normal and failing human hearts. Methods and Results —A whole-cell patch-clamp technique was used to measure ion currents in cardiomyocytes isolated from the left ventricle of explanted hearts from 10 patients with end-stage HF and from 3 normal hearts. We found I NaL was activated at a membrane potential of −60 mV with maximum density (0.34±0.05 pA/pF) at −30 mV in cardiomyocytes of both normal and failing hearts. The steady-state availability was sigmoidal, with an averaged midpoint potential of −94±2 mV and a slope factor of 6.9±0.1 mV. The current was reversibly blocked by the Na + channel blockers tetrodotoxin (IC 50 =1.5 μmol/L) and saxitoxin (IC 50 =98 nmol/L) in a dose-dependent manner. Both inactivation and reactivation of I NaL had an ultraslow time course (τ≈0.6 seconds) and were independent of voltage. The amplitude of I NaL was independent of the peak transient Na + current. Conclusions —Cardiomyocytes isolated from normal and explanted failing human hearts express I NaL characterized by an ultraslow voltage-independent inactivation and reactivation." @default.
• W2065355000 created "2016-06-24" @default.
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• W2065355000 date "1998-12-08" @default.
• W2065355000 modified "2023-10-01" @default.
• W2065355000 title "Novel, Ultraslow Inactivating Sodium Current in Human Ventricular Cardiomyocytes" @default.
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• W2065355000 doi "https://doi.org/10.1161/01.cir.98.23.2545" @default.
• W2065355000 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9843461" @default.
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