Open AccessExtracellular hypotonicity induces disturbance of sodium currents in rat ventricular myocytes
Author(s) -
Long Hu,
Jing Ma,
P Zhang,
Jie Zheng
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931692
Subject(s) - bisindolylmaleimide , tonicity , bapta , extracellular , chemistry , biophysics , sodium , intracellular , sodium channel , protein kinase c , patch clamp , medicine , myocyte , endocrinology , biochemistry , signal transduction , biology , receptor , organic chemistry
Hypotonic solution alters ion channel activity, but little attentionhas been paid to voltage-dependent sodium channels. The aim ofthis study was to investigate the effects of hypotonic solution ontransient sodium currents (INaT) and persistent sodium currents(INaP). We also explored whether the intracellular signaltransduction systems participated in the hypotonic modificationsof sodium currents. INaT and INaP were recorded by means ofwhole-cell patch-clamp technique in isolated rat ventricularmyocytes. Our results revealed that hypotonic solution reducedINaT and simultaneously augmented INaP with the occurrence ofinterconversion between INaT and INaP. Hypotonic solution shiftedsteady-state inactivation to a more negative potential, prolongedthe time of recovery from inactivation, and enhancedintermediate inactivation (IIM). Ruthenium red (RR, inhibitor ofTRPV4), bisindolylmaleimide VI (BIM, inhibitor of PKC), Kn-93(inhibitor of Ca/CaMKII) and BAPTA (Ca2+-chelator) inhibited theeffects of hypotonic solution on INaT and INaP. Therefore weconclude that hypotonic solution inhibits INaT, enhances INaP andIIM with the effects being reversible. TRPV4 and intracellular Ca2+,PKC and Ca/CaMKII participate in the hypotonic modifications ofsodium currents.