Chiba S, Tsukada M
Jpn J Pharmacol. 1986 Sep;42(1):141-4. doi: 10.1254/jjp.42.141.
Effects of angiotensin II on norepinephrine- and KCl-induced vasoconstrictions were investigated in isolated canine mesenteric arteries which were perfused with Krebs' solution at 37 degrees C. Angiotensin Ii at 0.03-0.3 microgram showed tachyphylaxis in the injection intervals used (10, 20 or 30 min intervals). After treatment with angiotensin II (0.18-1.8 microgram), norepinephrine- and KCl-induced constrictions were consistently potentiated. Imipramine which blocked tyramine-induced action did not significantly influence norepinephrine-induced constriction. pretreatments with both angiotensin II and indomethacin enhanced norepinephrine-induced constriction much greater than that with angiotensin II alone. It is suggested that angiotensin II may modify intracellular Ca movements and prostaglandin production induced by norepinephrine.
在37℃用 Krebs 溶液灌注的离体犬肠系膜动脉中,研究了血管紧张素II对去甲肾上腺素和氯化钾诱导的血管收缩的影响。在所用的注射间隔(10、20或30分钟间隔)中,0.03 - 0.3微克的血管紧张素II表现出快速耐受性。用血管紧张素II(0.18 - 1.8微克)处理后,去甲肾上腺素和氯化钾诱导的收缩持续增强。阻断酪胺诱导作用的丙咪嗪对去甲肾上腺素诱导的收缩没有显著影响。血管紧张素II和吲哚美辛预处理比单独使用血管紧张素II更能增强去甲肾上腺素诱导的收缩。提示血管紧张素II可能改变去甲肾上腺素诱导的细胞内钙运动和前列腺素生成。