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α<sub>2</sub>-Adrenoceptor Agonists의 흰쥐 대동맥 이완 작용
조인국,이상우,강형섭,서형석,김진상,Cho, In-gook,Lee, Sang-woo,Kang, Hyung-sub,Seo, Heyng-seok,Kim, Jin-shang 대한수의학회 2003 大韓獸醫學會誌 Vol.43 No.3
The vasorelaxant actions and blood pressure lowering of the ${\alpha}_2$-adrenoceptor agonists (${\alpha}_2$-AAs) clonidine and xylazine were investigated in rat isolated aortic rings and anesthesized rats. Both clonidine and xylazine produced a concentration-dependent inhibition of the sustained contraction induced by norepinephrine (NE), but not by KCl. NE-induced contractions were attenuated partly by nifedipine or verapamil, voltage dependent $Ca^{2+}$ channel blockers. These $Ca^{2+}$ channel blockers-resistant contractions were abolished by clonidine or xylazine. Inhibitory effects of a ${\alpha}_2$-AAs on contractions could be reversed by ryanodine, an intracellular $Ca^{2+}$, transport blocker, and tetrabutylammonium (TBA), a $Ca^{2+}$ activated $K^+$ channel blocker, but not by nifedipine, glibenclamide or removal of extracellular $Ca^{2+}$ and endothelium. Moreover, ${\alpha}_2$-AAs produced relaxation in NE-precontracted isolated intact aortic rings in a concentration-dependent manner, but not in KCl-precontracted rings. The relaxant effects of ${\alpha}_2$-AAs were inhibited by ryanodine and TBA, but not by nifedipine, glibenclamide, N (G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG), 2-nitro-4-carboxyphenyl N,N-diphenylcarhurnte (NCDC), lithium sulfate, staurosporine or removal of extracellular $Ca^{2+}$ and endothelium. In vivo, infusion of xylazine elicited significant decrease in anerial blood pressure. This xylazinelowered blood pressure was completely inhibited by the intravenous injection of TBA, but not by the intravenous injection of glibenclamide, L-NNA, L-NAME, AG, nifedipine, lithium sulfate or saponin.. These findings showed that the receptor-mediated and ${\alpha}_2$-adrenoceptor A-stimulated endothelium-independent vasorelaxant effect may be explained by decreasing intracellular $Ca^{2+}$ release and activation of $Ca^{2+}$-activated $K^+$ channels, which may contribute to the hypotensive effects of ${\alpha}_2$-AAs in rats.
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흰쥐 대동맥에서 melatonin의 내피 의존적 혈관 이완 작용에 대한 lithium의 영향
김상진,유선봉,조인국,강형섭,김진상,Kim, Shang-Jin,Yu, Xianfeng,Cho, In-Gook,Kang, Hyung-Sub,Kim, Jin-Shang 대한수의학회 2005 大韓獸醫學會誌 Vol.45 No.4
Melatonin, the principal hormone of the vertebral pineal gland, participates in the regulation of cardiovascular system in vitro and in vivo. Lithium inhibits both inositol polyphosphate phosphatase (IPPase) and inositol monophosphatase (IMPase), which are involved in a wide range of signal transduction pathways. The aim of the present study was to assess the effect of lithium on endothelial-dependent relaxation to melatonin and on the melatonin-induced inhibition of contraction by phenylephrine (PE) in isolated rat aorta. Melatonin induced a concentration-dependent relaxation in PE-precontracted in endothelium-intact (+E) aortic rings. Melatonin inhibited a PE-induced sustained contraction in +E aortic rings. These effects of melatonin on relaxation and contractile responses were inhibited by pretreatment with lithium. In PE-precontracted +E aortic rings, the melatonin-induced vasorelaxations and the inhibitory effects of melatonin on maximal contractions were inhibited by endothelium removal or by pretreatment with L-$N^G$-nitro-arginine (L-NNA), 1H-[1,2,4] oxadiazolo-[4,3-a] quinoxalin-1-one (ODQ) and nifedipine and verapamil, but not by tetrabutylammonium, clotrimazole and glibenclamide, However, in endothelium-denuded (-E) aortic rings and in the presence of L-NNA and ODQ in +E aortic rings, the melatonin-induced residual relaxations and the melatonin-induced residual contractile responses to PE were not affected by lithium. It is concluded that the inositol phosphate pathway may be involved in endothelial-dependent relaxation induced by melatonin.
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