These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Electrophysiological effects of phytoestrogen genistein on pacemaker cells in sinoatrial nodes of rabbits.
    Author: Ma T, Fan ZZ, He RR.
    Journal: Acta Pharmacol Sin; 2002 Apr; 23(4):367-70. PubMed ID: 11931696.
    Abstract:
    AIM: To study the electrophysiological effects of genistein (GST) on pacemaker cells in sinoatrial (SA) nodes of rabbits. METHODS: Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique. RESULTS: GST (10 - 150 micromol/L) not only decreased the amplitude of action potential (APA), maximal rate of depolarization (Vmax) [from (6.2 +/- 2.8) to (2.8 +/- 1.4) V/s, P < 0.01], velocity of diastolic (phase 4) depolarization (VDD) [from (55 +/- 14) to (38 +/- 8) mV/s, P < 0.01], and rate of pacemaker firing (RPF) [from (154 +/- 23) to (107 +/- 25) beat/min, P < 0.01], but also prolonged duration of 90 % repolarization of action potential (APD90) in a concentration-dependent manner. Both elevation of calcium concentration (5 mmol/L) in superfusate and application of L-type Ca2+ channel agonist Bay K8644 (0.5 micromol/L) reversed the inhibitory effects of GST on pacemaker cells, while pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 1 mmol/L), an NO synthase inhibitor, failed to block the electrophysiological effects of GST. CONCLUSION: GST exerted a negative chronotropic action and induced a delayed repolarization of pacemaker cells in SA nodes of rabbits. These effects were likely due to reduction in calcium influx and potassium efflux, but had no association with NO release.
    [Abstract] [Full Text] [Related] [New Search]