Key Points
- To investigate the regulatory effects of insulin-like growth factor I (IGF-I) on cardiac potassium channel expression and currents in cultured neonatal rat ventricular myocytes.
- Cultured neonatal rat ventricular myocytes were treated with 60 ng/ml IGF-I for 72 hours to evaluate hypertrophy and ion channel remodeling.
- Whole-cell patch-clamp electrophysiology characterized outward K+ currents alongside sensitivity to 4-aminopyridine, isoproterenol, and tetraethylammonium.
- Single-cell immunofluorescence using an antibody targeting the COOH terminus of the Kv1.5 channel protein was performed following voltage-clamp recordings.
- Identified two 4-aminopyridine-sensitive outward currents: a predominant transient current (IC50 = 0.87 mM) and an ultrarapid delayed rectifier-like current (IC50 = 66.5 µM) enhanced by isoproterenol.
- Treatment with IGF-I for 72 hours stimulated myocyte hypertrophy and increased the proportion of cells expressing the ultrarapid delayed rectifier current alone or in combination with the transient outward current.
- Single myocytes pretreated with IGF-I that displayed larger ultrarapid currents exhibited significantly stronger immunofluorescent labeling for Kv1.5 channel protein.
Structured PICO
Does IGF-I regulate K(+)-channel expression in cultured neonatal rat ventricular myocytes?
PPopulationCultured neonatal rat ventricular myocytes
IIntervention72-hour exposure to 60 ng/ml Insulin-like growth factor (IGF) I
OOutcomeCardiac K(+)-channel expression (Ito and IKur) and myocyte hypertrophysurrogate
IGF-I regulates K(+)-channel expression in cultured neonatal rat ventricular myocytes, providing insight into its role in modulating cardiac excitability.