Electrophysiologic effect of moxonidine on action potential in rabbit sinoatrial node pacemaker cells

AIM To explain the mechanism of moxonidine(Mox) in treatment of experimental arrhythmia by studying whether Mox has the electrophysiologic effects on sinoatrial node(SAN) pacemaker cells and which are its related receptors. METHODS Intracellular microelectrode technique was used to record action potentials(AP) in the rabbit SAN pacemaker cells. RESULTS Mox (0.3-3.0 mmol·L -1) concentration-dependently decreased the velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF),and prolonged the duration at 50% and 90% repolarization (APD 50 and APD 90) of AP in the rabbit SAN pacemaker cells. Mox at 1.0 and 3.0 mmol·L -1 significantly increased maximal diastolic potential (MDP). The effects of Mox on VDD, APD 50 and APD 90 were inhibited completely by yohimbine (1.0 μmol·L -1 pre-perfused for 20 min), while those on RPF and MDP were inhibited by yohimbine at lower concentration of Mox. Moreover, in the preparations pre-treated with yohimbine, Mox increased AP amplitude and maximal depolarization rate of phase 0 ( max) significantly. CONCLUSION Mox prolongs the APD 50 and APD 90, and decreases the VDD in the rabbit SAN pacemaker cells, which are mainly mediated by α 2-adrenoceptors. In addition, the effects of Mox on MDP and RPF are partially mediated by α 2-adrenoceptors.