ASSA13-03-46 The Effects of Verapamil On SK2 Channel In Myocardium Cells From Human Chronic Atrial Fibrillation

Abstract

<h3>Objective</h3> Small conductance calcium-activated potassium channel (SK channel) plays an important role in heart. Four subtype of SK channel are classified according to their sensitive to apamin. Electrophysiological properties of SK2 channel are voltage-independent as well as solely activated by changes in intracellular calcium concentration. This study investigated the alteration of SK2 channel currents in cAF patients. Moreover, L-type calcium channel inhibitor verapamil were adopted to observe the change of SK2 channel. We plan to explore the functional relationship between L-type calcium channel and SK2 channels. <h3>Methods</h3> Single human cardiac myocyte was isolated by two-step enzyme digestion. The whole-cell patch clamp technique was used to record the SK2 current in isolated cardiomyocytes from patients with siuns rhythm (SR) or chronic atrial fibrillation (cAF). Verapamil (10 μmol/L) and apamin (100 nmol/L) were added into bath solution respectively to observe the change of current. <h3>Results</h3> The current density (pA/pF) of SK2 channel as well as the ration in the integrated inward currents were up-regulated significantly in cAF groups. At wide range of test potentials, L-type calcium channel inhibitor verapamil reduced SK2 channel currents in cardiomyocytes from patients with SR or cAF. Compared with control group, the apamin-sensitive currents density of the verapamil group showed a significant decrease in human atrial myocytes. It indicates that part of SK2 current can be inhibited by verapamil. <h3>Conclusions</h3> It suggested that the up-regulation of SK2 currents underlies the occurrence and maintenance of cAF. There may be functionally coupling between SK2 channels and L-type calcium channels in human myocardium cells. The regulation of L-type calcium channel involves the remodelling of SK2 channels in the atrial myocytes from SR and cAF patients. This work was supported by the National Natural Science Foundation of China (No. 30870903) and the Natural Science Foundation of Luzhou.