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1 University Francois-Rabelais Tours
* To whom correspondence should be addressed. E-mail: findlay{at}univ-tours.fr.
Ectopic activity in cardiac muscle within pulmonary veins is associated with the onset and the maintenance of atrial fibrillation in man. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat pulmonary vein. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat pulmonary vein (PV) and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV (-70±1 mV, mean ±SE, n=8) than in LA (-85±1 mV, n=8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10-5M) induced first a hyperpolarisation (-8±1 mV in PV: -3±1 mV in LA: n=8 for both) then a slowly developing depolarisation (+21±2 mV after 15 min in PV: +1±2 mV in LA) of the resting membrane potential. Automatic activity occurred only in PV, it was triggered at ~-50 mV and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarised between bursts. Automatic activity in the PV was blocked by either atenolol or prazosine and it could be generated with a mixture of cirazoline and isoprenaline. In both tissues cirazoline (10-6M) induced a depolarization (+37±2 mV in PV, n=5: +5±1 mV in LA, n=5) and isoprenaline (10-7M) evoked a hyperpolarisation (-11±3 mV in PV, n=7: -3±1 mV in LA, n=6). The differences in membrane potential and reaction to adrenergic stimulation lead to automatic electrical activity occurring specifically in cardiac muscle in the PV.
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