Superoxide anion and K+ channels mediate electrical stimulation-induced relaxation in the rat basilar artery.

Electrical field stimulation (a single pulse, 0.2 ms) caused a rapid relaxation of rat basilar artery segments precontracted with different agents, but not with 30 mM KCl. This relaxation was not modified by endothelium removal, 10 microM tetrodotoxin, 1 microM propranolol, 1 microM atropine, 30 microM indomethacin, 10 microM methylene blue, 100 microM N(G)-nitro-L-arginine methyl ester or 1 microM cimetidine but it was significantly reduced by 50 and 100 U/ml superoxide dismutase. Charybdotoxin (0.1 and 0.2 microM), a blocker of large-conductance Ca2+-activated K+ channels (BK(Ca)), decreased the relaxation elicited by electrical stimulation, whereas it was unaltered by 10 microM glibenclamide or 1 microM apamin, blockers of ATP-sensitive (K(ATP)) or small-conductance K(Ca) channels, respectively. Thapsigargin (0.01 and 0.1 microM), an inhibitor of sarcoplasmic reticulum Ca2+-ATPase, increased the electrical stimulation-induced relaxation, which was nearly abolished by charybdotoxin. These results show that electrical stimulation induces endothelium-independent and non-neurogenic relaxations in the rat basilar artery. This response appears to involve generation of superoxide anion, increase of cytosolic free Ca2+ concentration and subsequent activation of BK(Ca) channels.