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Effects of salvianolic acid B on L-type calcium channels and myocardial contractility in isolated rat ventricular myocytes and hERG K+ channels expressed in HEK293 cells

Effects of salvianolic acid B on L-type calcium channels and myocardial contractility in isolated... Salvianolic acid B (Sal B), one of the chief water-soluble constituents in Radix Salviae Milthiorrhizae, has often been reported to possess considerable cardiovascular regulatory effects. However, the underlying biochemical and cellular mechanisms of its cardioprotection remain unclear. This study was designed to evaluate the role of Sal B regulation in L-type Ca2+ channel currents (ICa,L) and cell contractility in rat cardiomyocytes and hERG K+ channels expressed in HEK293 cells with the patch-clamp and Ca2+ imaging techniques to clarify its underlying cardioprotective mechanisms. Exposure to Sal B blocked ICa,L with IC50 of 2.07 × 10−5 M, shifted the curves of current and voltage upwards, shifted the curves of activation and inactivation to the left, and significantly inhibited the amplitude of the cell shortening, but the regulatory effects of Sal B on the expressed rapidly activating delayed rectifier potassium current (IKr) did not reach a significant level. These results indicate that the cardioprotective mechanisms of Sal B may be related to the attenuation of calcium overload by directly inhibiting ICa,L and consequently decreasing myocardial contractility without causing drug-induced long QT syndrome (LQTS). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Naunyn-Schmiedeberg's Archives of Pharmacology Springer Journals

Effects of salvianolic acid B on L-type calcium channels and myocardial contractility in isolated rat ventricular myocytes and hERG K+ channels expressed in HEK293 cells

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References (39)

Publisher
Springer Journals
Copyright
Copyright © 2017 by Springer-Verlag Berlin Heidelberg
Subject
Biomedicine; Pharmacology/Toxicology; Neurosciences
ISSN
0028-1298
eISSN
1432-1912
DOI
10.1007/s00210-017-1381-4
pmid
28477086
Publisher site
See Article on Publisher Site

Abstract

Salvianolic acid B (Sal B), one of the chief water-soluble constituents in Radix Salviae Milthiorrhizae, has often been reported to possess considerable cardiovascular regulatory effects. However, the underlying biochemical and cellular mechanisms of its cardioprotection remain unclear. This study was designed to evaluate the role of Sal B regulation in L-type Ca2+ channel currents (ICa,L) and cell contractility in rat cardiomyocytes and hERG K+ channels expressed in HEK293 cells with the patch-clamp and Ca2+ imaging techniques to clarify its underlying cardioprotective mechanisms. Exposure to Sal B blocked ICa,L with IC50 of 2.07 × 10−5 M, shifted the curves of current and voltage upwards, shifted the curves of activation and inactivation to the left, and significantly inhibited the amplitude of the cell shortening, but the regulatory effects of Sal B on the expressed rapidly activating delayed rectifier potassium current (IKr) did not reach a significant level. These results indicate that the cardioprotective mechanisms of Sal B may be related to the attenuation of calcium overload by directly inhibiting ICa,L and consequently decreasing myocardial contractility without causing drug-induced long QT syndrome (LQTS).

Journal

Naunyn-Schmiedeberg's Archives of Pharmacology – Springer Journals

Published: May 5, 2017

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