Objective: 

Much attention is paid to the pulmonary veins (PVs) myocardium as a region responsible for activity triggering atrial fibrillation. However, only several studies dedicated on electrophysiology of rat PVs myocardium. The aim of the present study is to investigate effects of acetylcholine (ACh) and beta-adrenoreceptors agonist isoproterenol (ISO) on membrane potential of rat PVs myocardium.

Methods: 

Multicellular preparations including part of left atria and PV of left lung lobe were dissected from male Wistar (200–250 g) rats hearts. Resting (RP) and action potentials (APs) were recorded from left atria appendage (LAA, control) and proximal part of PV with use of standard microelectrode technique. RP (and APs) were recorded in electrically paced and quiescent preparations.

Results: 

Application of ACh (10 mM) and ISO (5 mM) induced slight hyperpolarization in LAA and in PV during pacing. In quiescent preparation (10 min after pacing termination) RP in PV region stabilized at level -60±5 mV. Application of ACh and ISO induced strong hyperpolarization (up to -87±2 and -73±4 mV respectively).

Hyperpolarization induced both by ACh and ISO in PV region of paced and quiescent preparations was practically fully abolished in presence of barium ions (50 mM, 5 min) - blocker of inward rectifier potassium channels. Automatic activity and afterdepolarizations were observed after barium application in PV region (but not in LAA) of ISO-treated preparations.

Conclusions: 

Both ACh and ISO induce hyperpolarization in the rat PVs myocardium. Application of barium leads to abolishing of drug-induced hyperpolarization. Thereby, ISO-induced hyperpolarization in rat PVs myocardium, probably, is mediated via activations of IK, ACh as in case of acetylcholine.