Hypoxia increases persistent sodium current in rat ventricular myocytes.

摘要: 1. A persistent inward current activated by depolarization was recorded using the whole-cell, tight seal technique in rat isolated cardiac myocytes. The amplitude of increased when cells were exposed to a solution with low oxygen tension. 2. had characteristics Na+ described previously ventricular myocytes: it at negative potentials (-70 mV), reversed close equilibrium potential for (ENa), blocked TTX and resistant inactivation. 3. Persistent single channel currents long (200-400 ms) depolarizations cell-attached patches on Hypoxia frequency opening channels. 4. channels during hypoxia similar those normal tensions. They null ENa, their varied [Na+], they inactivation mean open time increasing depolarization. 5. (50 microM) patch pipette lidocaine (100 microM). 6. It concluded that increases probability TTX-sensitive, inactivation-resistant voltage dependence these channels, greatly activity hypoxia, suggest may play an important role generation arrhythmias hypoxia.