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 mu M tetrodotoxin, 1 mu M propranolol, 1 mu M atropine, 30 mu M indomethacin, 10 mu M methylene blue, 100 mu M N-G-nitro-L-arginine methyl eater or 1 mu M cimetidine but it was significantly reduced by 50 and 100 U/ml superoxide dismutase. Charybdotoxin (0.1 and 0.2 mu M), a blocker of large-conductance Ca2+-activated K+ channels (BKCa), decreased the relaxation elicited by electrical stimulation, whereas it was unaltered by 10 mu M glibenclamide or 1 mu M apamin, blockers of ATP-sensitive (K-ATP) or small-conductance K-ATP channels, respectively. Thapsigargin (0.01 and 0.1 mu M), 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 fat basilar artery. This response appears to involve generation of superoxide anion, increase of cytosolic free Ca2+ concentration and subsequent activation of BKCa channels. (C) 1999 Elsevier Science B.V. All rights reserved.