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A high concentration of extracellular inorganic phosphate (Pi) causes an increase in membrane potential and may thus slow down the acquisition of antiarrhythmic drug tolerance (ADT). We therefore investigated whether exposure to high concentrations of Pi would influence ADT induced by drugs that affect ion channels. Atrial myocytes isolated from adult rats were superfused at 37 degrees C under whole cell voltage clamp for 15 min with different concentrations of Pi (0.1-10 mm). Excitability threshold and action potential duration (APD) at 0.2, 0.5 and 1.0 Hz were determined under control conditions and in the presence of ADT induced by 4-aminopyridine (4-AP) and lidocaine. The membrane was then depolarized to a steady-state potential of 0 mV for 15 min and the same experiments were repeated. Both 4-AP and lidocaine were more effective in increasing excitability threshold during the control period and during the steady-state potential of 0 mV than during the pre-adaptation period. A high concentration of Pi (4 mm) attenuated the 4-AP-induced increase in
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