Electrophysiological effects of phytoestrogen genistein on spontaneous activity of rabbit atrioventricular node cells

The purpose of this study was to determine the electrophysiological effects of genistein (GST) on spontaneous activity of atrioventricular (AV) node and the underlying mechanism(s). Action potentials in AV node cells were recorded using intracellular microelectrode technique. GST not only reduced the amplitude of action potential (APA), maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization (VDD), and rate of spontaneous firing (RSF), but also prolonged 90% duration of action potential (APD(90)) in a concentration-dependent manner. The effects of GST (50 micromol/L) could be blocked completely by pretreatment with Bay K8644 (0.25 micromol/L), an agonist of L-type calcium channel. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 0.5 mmol/L), a nitric oxide (NO) synthase inhibitor, did not affect the effects of GST on AV node cells. Elevation of Ca(2+) concentration (5 mmol/L) in superfusate antagonized the effects of GST (50 micromol/L). These results suggest that GST exerted a negative electrophysiological effects of spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but had no association with NO release.