4-Aminopyridine attenuates endothelium-derived hyperpolarizing factor-induced hyperpolarization and relaxation of rat mesenteric small arteries (part 6)
Tetrodotoxin (10-6 M) and atropine (10-6 M) did not affect carbachol-induced SMC hyperpolarization or tension decrease of mesenteric arteries in normal PSS, or in the presence of LNNA and indomethacin. These data suggest that nerve terminals do not participate in carbachol-induced SMC hyperpolarization and vessel relaxation. Shop with best online pharmacy and find proventil albuterol getting the most out of it.
In vitro application of carbachol did not cause noticeable force changes in intact resting mesenteric arteries but produced relaxation of these vessels preconstricted with noradrenaline. A possible explanation is lack of myogenic tonus in the small branches of rat mesenteric arteries. This hypothesis is confirmed in our experiments by the lack ofvessel wall relaxation on exposure to Ca2+-free (EGTA 1 mM) solution. 4-AP reduced but did not block carbachol-induced hyperpolarization of SMC and relaxation of preconstricted mesenteric arteries in normal PSS. This result implies that not only 4-AP-sensitive potassium currents are responsible for hyperpolarization of SMC membrane when all relaxing factors are released from endothelium; ATP-sensitive potassium channels and Na+/K+ exchange have also been shown to participate in hyperpolarization of SMC isolated from rat mesenteric arteries at these membrane potentials .