Effects of hydrogen sulfide on guinea pig aortic vestibule autorhythmic cells electrophysiology and its mechanism

Objective: To investigate the electrophysiological effects of hydrogen sulfide (H2S) on left ventricular outflow tract autonomic cells in guinea pigs and its mechanism. Methods: Intracellular microelectrode recording technique was used to observe the electrophysiological effects of different conc...

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Bibliographic Details
Main Author: Ling Fan
Format: Article
Language:English
Published: Editorial Board of Journal of Hainan Medical University 2019-02-01
Series:Journal of Hainan Medical University
Online Access:http://www.hnykdxxb.com/PDF/201904/03.pdf
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Summary:Objective: To investigate the electrophysiological effects of hydrogen sulfide (H2S) on left ventricular outflow tract autonomic cells in guinea pigs and its mechanism. Methods: Intracellular microelectrode recording technique was used to observe the electrophysiological effects of different concentrations of hydrogen sulfide on the autonomic cells of left ventricular outflow tract. Results: CSE irreversible inhibitor PPG (200 μmol/L) makes the left ventricular outflow tract of autorhythmic cells Vmax, RPF and VDD accelerate, APA increase (P< 0.05); CBS synthase inhibitor AOAA (100μmol/L) acts on the autorhythmic cells of the left ventricular outflow tract without effect. The concentration-dependency of the 50, 100 and 200 μmol/L NaHS made RPF and VDD of autorhythmic cell of the left ventricular outflow tract decrease with increasing concentration of NaHS, Vmax and APA decrease (P<0.01). The ATP sensitive potassium channel (KATP) blocker glybenclamide (Gli, 20 μmol/L) partially blocked the electrophysiological effects of NaHS (P<0.05). The L-Ca2+ channel agonist Bay K8644 could partially block the electrophysiological effects of NaHS. Conclusion: The autorhythmic cells of the left ventricular outflow tract had endogenous H2S produced by CSE. H2S had a negative chronotropic effect on autorhythmic cells in the left ventricular outflow tract, and its mechanism was related to the inhibition of L-Ca2+ channels by the open KATP pathway.
ISSN:1007-1237
1007-1237