Şahin, A. S.Atalık, K. E.Günel, E.Doğan, N.2020-03-262020-03-2620010379-0355https://dx.doi.org/10.1358/mf.2001.23.1.619174https://hdl.handle.net/20.500.12395/17578The aim of the present study was to investigate the possible role of notric oxide (NO) as a nonadrenergic, noncholinergic (NANC) mediator in human colon smooth muscle in vitro and to examine its possible interactions with K+ channels. In the presence of atropine (10(-6) M) and guanethidine (10(-5)M).. electrical field stimulation (EFS, 1-10 Hz, 0.3 msec, 50V) for 10 sec induced relaxations which were inhibited by tetrodotoxin (10(-6) M). in the presence of N-G-nitro-L-arginine methyl ester (L-NAME, 10(-4) M), relaxations induced by EFS at 1, 2, 4, 8 and 10 Hz were reduced by 38.7 +/- 4.3, 31.5 +/-3.8, 54.3 +/-5.4, 59.8 +/- 4.5 and 68.6 +/- 5.3% respectively. THe relaxations inhibited by L-NAME were restored by the preincubation of L-argarinine (L-ARG, 10(-3) M) at all frequencies tested. D-Arginine (D-ARG, 10(-3) M) had no effect. Tetraethylammonium (TEA, 10(-4) M) or glibenclamidine (10(-6) M) significantly decreased the relaxations induced induced by EFS. Exogenously applied sodium nitroprusside caused concentration-dependent relaxation with prusside. In conclusion, our data indicate that NO is involved in NANC nerve-mediated relaxation in the human calcium-dependent and ATP-sensitive K+ channels.en10.1358/mf.2001.23.1.619174info:eu-repo/semantics/openAccessHuman ColonIn vitroK+ ChannelsNonadrenergic-Noncholinergic ResponsesArticle231131711413858N/AWOS:000169090300002Q4