학술논문
Extracellular hypotonicity induces disturbance of sodium current in rat ventricular myocytes
Document Type
TEXT
Source
Subject
Language
English
Multiple Languages
Multiple Languages
Abstract
L. Hu ... [et al.].
Obsahuje seznam literatury
Hypotonic solution alters ion channel activity, but little attention has been paid to voltage-dependent sodium channels. The aim of this study was to investigate the effects of hypotonic solution on transient sodium currents (INaT) and persistent sodium currents (INaP). We also explored whether the intracellular signal transduction systems participated in the hypotonic modifications of sodium currents. INaT and INaP were recorded by means of whole-cell patch-clamp technique in isolated rat ventricular myocytes. Our results revealed that hypotonic solution reduced INaT and simultaneously augmented INaP with the occurrence of interconversion between INaT and INaP. Hypotonic solution shifted steady-state inactivation to a more negative potential, prolonged the time of recovery from inactivation, and enhanced intermediate inactivation (IIM). Ruthenium red (RR, inhibitor of TRPV4), bisindolylmaleimide VI (BIM, inhibitor of PKC), Kn-93 (inhibitor of Ca/CaMKII) and BAPTA (Ca2+-chelator) inhibited the effects of hypotonic solution on INaT and INaP. Therefore we conclude that hypotonic solution inhibits INaT, enhances INaP and IIM with the effects being reversible. TRPV4 and intracellular Ca2+, PKC and Ca/CaMKII participate in the hypotonic modifications of sodium currents.
Obsahuje seznam literatury
Hypotonic solution alters ion channel activity, but little attention has been paid to voltage-dependent sodium channels. The aim of this study was to investigate the effects of hypotonic solution on transient sodium currents (INaT) and persistent sodium currents (INaP). We also explored whether the intracellular signal transduction systems participated in the hypotonic modifications of sodium currents. INaT and INaP were recorded by means of whole-cell patch-clamp technique in isolated rat ventricular myocytes. Our results revealed that hypotonic solution reduced INaT and simultaneously augmented INaP with the occurrence of interconversion between INaT and INaP. Hypotonic solution shifted steady-state inactivation to a more negative potential, prolonged the time of recovery from inactivation, and enhanced intermediate inactivation (IIM). Ruthenium red (RR, inhibitor of TRPV4), bisindolylmaleimide VI (BIM, inhibitor of PKC), Kn-93 (inhibitor of Ca/CaMKII) and BAPTA (Ca2+-chelator) inhibited the effects of hypotonic solution on INaT and INaP. Therefore we conclude that hypotonic solution inhibits INaT, enhances INaP and IIM with the effects being reversible. TRPV4 and intracellular Ca2+, PKC and Ca/CaMKII participate in the hypotonic modifications of sodium currents.