Abstract
Electrical field stimulation (EFS) caused biphasic relaxation, first transient and then sustained, of rat mesenteric arteries precontracted by prostaglandin (PG) F2α. The transient relaxation was reduced about 45%, and the sustained relaxation was not observed after endothelium denudation of the arteries. Nω-Nitro-L-arginine (L-NOARG) inhibited the biphasic relaxation induced by EFS. At 1 - 100 μM, L-NOARG inhibited the transient relaxation more than the sustained relaxation. Methylene blue inhibited the biphasic relaxation and at 100 μM, L-NOARG abolished the transient relaxation. These results suggest that the transient relaxation mainly involves nitric oxide (NO), whereas the sustained relaxation involves both NO and some other factor(s).
