백서 대동맥 평활근의 Acetylcholine 이완반응에서 K^+ Channel의 역할 = Role of K^+-Channel in Vasorelaxation induced by Acetylcholine in the Aorta of Rat

다국어 초록 (Multilingual Abstract)

To investigate whether the endothelium-dependent relaxation by acetylcholine (ACh) is due to the activation of K^+ channel, and what kind of K^+ channel plays an important role in vasorelaxation, the effects of K^+ channel blocker(glibenclamide, tetraethylammonium) were observed on the ACh-, sodium nitroprusside (SNP)- or 8-bromoguanosine 3' 5' -cyclic monophsphate (8-br-cGMP)-induced vasorelaxation in the rat thoracec aortic ring.
In the aortic rings precontracted with 10^6 M norepinephrine (NE), ACh (10^9 ~ 10^5 M) and SNP (10^10 ~ 10^6 M) produced a dose-dependent relaxation. The relaxation by ACh was completely inhibited by 1065 M methylene blue (MB), an inhibitor of guanylate cyclase, as well as 10^4 M N^w -nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of nitric oxide synthase. However, the relaxant response by SNP was decreased only by MB. Glibenclamide (10^5 M) had no significant effect on relaxant response to ACh or SNP. However, TEA (5 mM) inhibited the ACh- or SNP-induced relaxation significantly. 8-br-cGMP-induced relaxation was also inhibited by TEA (5mM), not by glibenclamide.
From the above results, it is suggested that the activation of K_Ca channel via cGMP-dependent pathway plays a significant role in the regulation of endothelium-dependent relaxation by ACh.