The principal finding of this study was that flecainide can inhibit ICa,L in isolated rabbit AVN myocytes. Relatively few studies have investigated the actions of flecainide on ICa,L, and this is the first study to characterize the actions of flecainide on any membrane current in the AVN. Class I anti-arrhythmics are thought to exert their action primarily via inhibition of sodium channels . Thus, the antiarrhythmic action of flecainide has been ascribed to its use-dependent blocking action on channels for INa .However, the effects of flecainide do not appear to be restricted to sodium channels. For example, the drug also inhibits the transient outward potassium current in canine and rabbit atrium and delayed rectifier potassium current . Moreover, previous studies, performed on myocytes from different species, suggest that flecainide may also affect ICa,L. Such studies offer a useful basis for comparison with the present data.
Scamps et al first investigated the effects of fle-cainide on cardiac ICa,L. Using frog ventricular myocytes, they found a dose- and voltage-dependent inhibitory action of this agent on ICa,L. They observed half-maximal inhibition of ICa,L at 20 pM, reported a voltage-dependent blocking effect and saw a shift of the current-voltage relation by 5 to 10 mV in the hyperpolarizing direction. Our data are in good agreement with those of Scamps et al. We saw clear dose-and voltage-dependent effects of this agent on rabbit AVN ICa,L and observed not only a decrease in ICa,L amplitude, but also a statistically significant hyperpolarizing shift in the voltage dependence of current activation. Most advantageous shopping – buy cheap antibiotics for everyone to spend less.