Fig. 4.
H2O2 activates small-conductance Ca2+-activated K+ (SKCa) channels, large-conductance Ca2+-activated K+ (BKCa) channels, and voltage-activated K+ channel 7 (Kv7) to blunt myogenic contractions. The reduction in luminal diameter with PP was inhibited by H2O2, but the effect of H2O2 was lessened by blockade of SKCa and BKCa channels with apamin (10−7 mol/l) and charybdotoxin (10−8 mol/l) (A) or blockade of Kv7 by linopirdine (10−5 mol/l; B) and was prevented by blockade of all channels by a combination of all three blockers (C). The increase in Em by H2O2 was prevented by blockade of K+ channels. DiBAC4(3) fluorescence was decreased with H2O2 (10−5 mol/l) (implying hyperpolarization), but this effect of H2O2 was lessened by apamin (10−7 mol/l) and charybdotoxin (10−8 mol/l; D) or linopirdine (10−5 mol/l; E) and prevented by a combination of all three blockers (F). *P < 0.05, **P < 0.01, and ***P < 0.005 compared with vehicle; †P < 0.05, ††P < 0.01, and †††P < 0.005 compared with H2O2 alone; ‡P < 0.05 and ‡‡‡P < 0.005 compared with antagonists alone.