Figure 3
SHH reduces action potential duration.
(A) Representative traces of action potential recorded in control and after SHH treatment (left panel) and in the presence the ATP-dependent potassium channel inhibitor glibenclamide (1 μM) (right panel). (B) Average values of resting membrane potential in control (n = 7), SHH (n = 8), Control+glibenclamide (n = 7), N-SHH+glibenclamide (n = 8), N-SHH+L-NNA (n = 7), N-SHH+L-NNA+glibenclamide (n = 7), N-SHH+ODQ (n = 7), N-SHH+ODQ+Glibenclamide (n = 7). (C) Action potential duration at 95% of the repolarization (APD95,) in control (n = 7), SHH (n = 8), Control+glibenclamide (n = 7), N-SHH+glibenclamide (n = 8), N-SHH+L-NNA (n = 7), N-SHH+L-NNA+glibenclamide (n = 7), N-SHH+ODQ (n = 7), N-SHH+ODQ+Glibenclamide (n = 7). (D) The effect of glibenclamide (Glib) was further evaluated in vivo on the QT interval. Representative ECGs recorded in control (top), N-SHH (middle) and N-SHH+Glib (lower panel) treated animal. (E) Summary of the mean QTc value in each condition indicating the prevention of N-SHH effect in the presence of glibenclamide. (control n = 5, N-Shh n = 8, N-Shh+Glib n = 6, *, p < 0.05 compared to vehicle).
