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This Article Full Text Full Text (PDF) All Versions of this Article: 297/1/H102    most recent 00256.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Doisne, N. Articles by Findlay, I. PubMed PubMed Citation Articles by Doisne, N. Articles by Findlay, I.

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein

¹Centre National de la Recherche Scientifique FRE 3092, Faculté des Sciences, Université François-Rabelais and ²Laboratoire de Pharmacologie, Faculté des Sciences Pharmaceutiques, Université François-Rabelais, Tours, France

Submitted 16 March 2009 ; accepted in final form 4 May 2009

Ectopic activity in cardiac muscle within pulmonary veins (PVs) is associated with the onset and the maintenance of atrial fibrillation in humans. The mechanism underlying this ectopic activity is unknown. Here we investigate automatic activity generated by catecholaminergic stimulation in the rat PV. Intracellular microelectrodes were used to record electrical activity in isolated strips of rat PV and left atrium (LA). The resting cardiac muscle membrane potential was lower in PV [–70 ± 1 (SE) mV, n = 8] than in LA (–85 ± 1 mV, n = 8). No spontaneous activity was recorded in PV or LA under basal conditions. Norepinephrine (10^–5 M) induced first a hyperpolarization (–8 ± 1 mV in PV, –3 ± 1 mV in LA, n = 8 for both) then a slowly developing depolarization (+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 approximately –50 mV, and it occurred as repetitive bursts of slow action potentials. The diastolic membrane potential increased during a burst and slowly depolarized 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^–6 M) induced a depolarization (+37 ± 2 mV in PV, n = 5; +5 ± 1 mV in LA, n = 5), and isoprenaline (10^–7 M) evoked a hyperpolarization (–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.

atrium; norepinephrine; electrophysiology; atrial fibrillation; thoracic veins