Electrophysiologic effects of 17β-estradiol on pacemaker cells in sinoatrial nodes of rabbits.
To investigate the electrophysiological effects of 17β-estradiol on pacemaker cells in sinoatrial (SA) nodes of rabbits and the underlying mechanism, intracellular microelectrode technique was used to record action potential (AP) in SA node cells of rabbits. The results showed that: (1) 17β-estradiol (1, 10, 100 μmol/L) not only significantly decreased the amplitude of action potential (APA) and the maximal rate of depolarization (V(max)), but also decreased the velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) in a concentration-dependent manner. The AP duration at 50% repolarization (APD(50)) and at 90% repolarization (APD(90)) were prolonged. But the maximal diastolic potential (MDP) was not affected. (2) Pretreatment with tamoxifen (10 μmol/L), an inhibitor of estrogen receptor, did not block the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. (3) Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 μmol/L), a nitric oxide (NO) synthase inhibitor, completely abolished the electrophysiological effects of 17β-estradiol (10 μmol/L) on SA node cells. The results suggest that 17β-estradiol inhibits the electrophysiological activity of pacemaker cells in SA nodes of rabbits in a concentration-dependent manner possibly through a non-genomic mechanism related with NO.
D000200:Action Potentials; D000818:Animals; D055724:Electrophysiological Phenomena; D004958:Estradiol / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000187:drug effects*; D011817:Rabbits; D012849:Sinoatrial Node / Q000166:cytology*
D004958:Estradiol