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A novel Na+ channel agonist, dimethyl lithospermate B, slows Na+ current inactivation and increases action potential duration in isolated rat ventricular myocytes
Journal article   Open access   Peer reviewed

A novel Na+ channel agonist, dimethyl lithospermate B, slows Na+ current inactivation and increases action potential duration in isolated rat ventricular myocytes

Jin-Young Yoon, Sung-Hun Ahn, Hyuncheol Oh, Young-Sup Kim, Shi Yong Ryu, Won-Kyung Ho and Suk-Ho Lee
British journal of pharmacology, Vol.143(6), pp.765-773
10/25/2004
DOI: 10.1038/sj.bjp.0705969
PMCID: PMC1575928
PMID: 15504759
url
https://europepmc.org/articles/pmc1575928View
Published (Version of record) Open Access

Abstract

Voltage-gated Na + channel blockers have been widely used as local anaesthetics and antiarrhythmic agents. It has recently been proposed that Na + channel agonists can be used as inotropic agents. Here, we report the identification of a natural substance that acts as a Na + channel agonist. Using the patch-clamp technique in isolated rat ventricular myocytes, we investigated the electrophysiological effects of the substances isolated from the root extract of Salvia miltiorrhiza , which is known as ‘Danshen' in Asian traditional medicine. By the intensive activity-guided fractionation, we identified dimethyl lithospermate B (dmLSB) as the most active component, while LSB, which is the major component of the extract, showed negligible electrophysiological effect. Action potential duration (APD 90 ) was increased by 20 μ M dmLSB from 58.8±12.1 to 202.3±9.5 ms. In spite of the prolonged APD, no early after-depolarization (EAD) was observed. dmLSB had no noticeable effect on K + or Ca 2+ currents, but selectively affected Na + currents ( I Na ). dmLSB slowed the inactivation kinetics of I Na by increasing the proportion of slowly inactivating component without inducing any persistent I Na . The relative amplitude of slow component compared to the peak fast I Na was increased dose dependently by dmLSB (EC 50 =20 μ M ). Voltage dependence of inactivation was not affected by dmLSB, while voltage dependence of activation shifted by 5 mV to the depolarised direction. Since the APD prolongation by dmLSB did not provoke EAD, which is thought as a possible mechanism for the proarrhythmia seen in other Na + channel agonists, dmLSB might be an excellent candidate for a Na + channel agonist.
Cardiac myocyte electrophysiology inotropic agent lithospermate B Na+ channel agonist Papers

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