| Abstrakt: |
Fast sodium current (INa) provides depolarization of the working myocardium, determining the excitability of its cells and the propagation velocity of excitation. Disturbances of activation and inactivation of sodium channels can lead to the development of various arrhythmias. In most vertebrates, with the exception of mammals, INa has been studied rather poorly, including in birds, which are of great interest for comparative physiology. This work first considers the characteristics of fast sodium current in the myocardium of adult birds. Using patch clamp method, the authors registered INa in isolated atrial and ventricular cardiomyocytes of Japanese quail. The current had a higher amplitude (in comparison with other vertebrates) and quickly recovered after inactivation; the fast inactivation time constant of INa in atrial myocytes turned out to be lower than in ventricular cells. The parameters of steady-state activation and inactivation suggest that the sodium window current in the avian myocardium is less pronounced than in the mammalian myocardium. In quail ventricular cardiomyocytes, the late sodium current blocker ranolazine caused a slight decrease in the peak amplitude of INa and did not affect the inactivation kinetics but shifted the steady-state activation curve towards more negative potentials, shortened action potentials, and decreased maximum upstroke velocity. Thus, it can be assumed that these INa characteristics in the quail myocardium reflect the adaptation to the high heart rate in birds and may indicate possible differences in the structure and functioning of sodium channels in the hearts of birds and mammals. [ABSTRACT FROM AUTHOR] |
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