Sai Y, Okamura T, Amakata Y, Toda N
Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
Eur J Pharmacol. 1995 Aug 25;282(1-3):235-41. doi: 10.1016/0014-2999(95)00343-j.
Responses to angiotensin II, bradykinin and arginine vasopressin were compared in helical strips of canine pulmonary arteries and veins. Angiotensin II contracted the artery but relaxed the vein strip. The artery contraction was augmented by indomethacin and aspirin and was abolished by losartan. The vein relaxation was not affected by endothelium denudation but was abolished by the cyclooxygenase inhibitors, a prostaglandin I2 synthase inhibitor and losartan. The bradykinin-induced artery relaxation was inhibited by endothelium denudation, NG-nitro-L-arginine (L-NA) or indomethacin and abolished by their combined treatment. The vein relaxation produced by bradykinin was endothelium-independent and was abolished by indomethacin. Vasopressin produced a slight relaxation in the arteries, which was abolished by endothelium denudation and L-NA. The vein relaxation produced by vasopressin was abolished by endothelium denudation and combined treatment with L-NA and indomethacin. It may be concluded that (1) activation of angiotensin AT1 receptor subtype in smooth muscle produces contraction and also relaxation due to prostaglandin I2 release; the former predominates over the latter in the artery, whereas only the latter is operative in the vein, (2) the bradykinin-induced relaxation is due to nitric oxide (NO) from the endothelium and prostaglandin I2 from subendothelial tissues in the artery and solely to prostaglandin I2 in the veins, and (3) the vasopressin-induced relaxation is mediated by endothelial NO in the artery, and NO and prostaglandin I2 in the vein.
在犬肺动脉和肺静脉的螺旋条带中比较了对血管紧张素II、缓激肽和精氨酸加压素的反应。血管紧张素II使动脉收缩，但使静脉条带松弛。动脉收缩被吲哚美辛和阿司匹林增强，并被氯沙坦消除。静脉松弛不受内皮剥脱的影响，但被环氧化酶抑制剂、前列腺素I2合酶抑制剂和氯沙坦消除。缓激肽诱导的动脉松弛被内皮剥脱、NG-硝基-L-精氨酸（L-NA）或吲哚美辛抑制，并被它们的联合处理消除。缓激肽产生的静脉松弛不依赖内皮，并被吲哚美辛消除。加压素在动脉中产生轻微松弛，这被内皮剥脱和L-NA消除。加压素产生的静脉松弛被内皮剥脱以及L-NA和吲哚美辛的联合处理消除。可以得出结论：（1）平滑肌中血管紧张素AT1受体亚型的激活由于前列腺素I2释放而产生收缩和松弛；前者在动脉中比后者占优势，而在静脉中只有后者起作用，（2）缓激肽诱导的松弛在动脉中是由于内皮产生的一氧化氮（NO）和内皮下组织产生的前列腺素I2，而在静脉中仅由于前列腺素I2，以及（3）加压素诱导的松弛在动脉中由内皮NO介导，在静脉中由NO和前列腺素I2介导。
