Fig. 7.

Ondansetron (Ondan) unmasks apamin-sensitive small-conductance Ca²⁺-activated K⁺ current (I_KAS) upregulation in Anemonia sulcata II (ATX-II)-pretreated mouse hearts. A: ATX-II did not affect heterologously expressed small-conductance Ca²⁺-activated K⁺ (SK)2 current. A, left: representative steady-state whole cell current responses sequentially recorded from a wild-type Ca²⁺-activated K⁺ subfamily N member 2 (KCNN2)-transfected human embryonic kidney (HEK)-293 cell in the presence of 15 nmol/l ATX-II (trace a) and during subsequent incubation with 100 nmol/l apamin (trace b). The voltage-clamp protocol is shown in the inset. A, right: plot of whole cell current amplitude at 0 mV as a function of time for the cell on the left. Exposure to 15 nmol/l ATX-II (arrow a) did not alter current amplitude measured at a potential of 0 mV, whereas subsequent exposure to 100 nmol/l apamin (arrow b) instantaneously and almost completely suppressed whole cell outward current. Identical results were obtained in another SK2 cell. B: rows A–D show representative sequences of action potential duration at 80% repolarization (APD₈₀) distribution maps obtained from one heart each at baseline (a) and across three consecutive 15-min sessions (b−d) during which hearts were exposed to the drugs indicated. Right graphs show superimpositions of representative optical action potentials. Blebbistatin (10 µmol/l) was present throughout all experiments. PCL, pacing cycle length.