Effects of Exogenous Adiponectin on Ionic Currents and Calcium Transients in Rat Ventricular Cardiomyocytes

Background. Adiponectin modulates myocardial function, but its electrophysiological effects in ventricular cardiomyocytes remain insufficiently understood. Our previous observations of prolonged ventricular repolarization after adiponectin administration prompted the present investigation of the underlying changes in ionic currents and intracellular Ca²⁺ transients. Aim . To assess the effects of induced hyperadiponectinemia on transmembrane currents, action potentials, and Ca²⁺ transients in rat ventricular cardiomyocytes. Methods . Male Wistar rats received recombinant rat adiponectin through subcutaneous osmotic pumps for seven days (n = 20); sham-operated rats served as controls (n = 19). Serum adiponectin was measured by ELISA. Whole-cell patch clamp was performed in enzymatically isolated ventricular cardiomyocytes to record action potentials, fast sodium (I Na ), transient outward potassium (I to ), L-type calcium (I CaL ), and inward rectifier potassium (I K1 ) currents. Ca²⁺ transients were recorded using Fluo-4 during 1 Hz electrical stimulation. Results . Adiponectin administration increased serum adiponectin concentrations and prolonged ventricular action potential duration at 90% repolarization (75.7 ± 29.0 versus 48.2 ± 13.5 ms, mean ± SD; p = 0.019). Ito density decreased at + 60 mV (p = 0.042), whereas outward I K1 density increased at − 60 mV (p = 0.022). Peak I Na and I CaL densities did not differ significantly between groups, but fast and slow time constants of I CaL inactivation were reduced in the treated animals. Ca²⁺ transient amplitude, time to peak, and decay time constant showed no significant differences between the groups. Conclusion. Exogenous adiponectin reduces I to density, increases outward I K1 density, and accelerates I CaL inactivation, which collectively results in action potential prolongation in rat ventricular cardiomyocytes.