Figure 6.

Electrophysiology of I_Kr and action potentials in guinea pig atrial cardiomyocytes. (A) Experimental protocol: I_Kr tail currents and AP were measured in freshly isolated atrial myocytes from adult guinea pig heart under control conditions and after pre-exposure to lipotoxicity for 2 h. Exemplar I_Kr tail current traces measured in control cells (B) and lipotoxic cells in the absence (C) and presence of RAP (D). (E) Population I–V curves for I_Kr tail currents measured in control cells (black symbol and line), lipotoxic cells (red symbol and line) and in lipotoxic cells pre-treated with RAP (cyan symbol and line). (F) I_Kr tail current amplitude measured at +10 mV under the indicated conditions. Representative AP traces measured in control cells (G) and after pre-exposure to lipotoxicity (2 h, H) and lipotoxicity+RAP (I). Statistical analysis of APD₅₀ (J) and APD₉₀ (K) revealed that RAP partially rescued lipotoxicity-induced shortening of APD in atrial myocytes. Data were generated from cardiomyocytes from three guinea pigs. (* statistical significance at p < 0.05).