Angiotensin II-induced relaxation of vascular smooth muscle.
Angiotensin II-induced relaxation of vascular smooth muscle.
复制标题
血管紧张素 II 诱导血管平滑肌松弛。
DOI：
10.1159/000158382
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Webb,RC
中科院分区：
文献类型：
--
作者：
Webb,RC
本文研究了血管紧张素II(All)对狗、猪和兔血管平滑肌收缩张力的影响。将螺旋切开的肾静脉条安装在器官腔中，并记录等长收缩。应用10-8g/ml去甲肾上腺素(NE)引起静脉条收缩。随后加入5×10~(-8)g/ml均可引起三时相反应：(1)初始收缩(随后的收缩在所有物种中都是快速性的)；(2)收缩之后是去甲肾上腺素(NE)引起的收缩以下的松弛(随后的松弛反应在狗和猪静脉中是快速性的)；(3)从松弛恢复到去甲肾上腺素引起的收缩的水平。整个反应持续时间约为5分钟。当NE浓度改变收缩状态时，收缩幅度与NE收缩程度成反比。抑制钠泵(无钾溶液和哇巴因)和用普奈洛尔阻断β-肾上腺素能的条件对All诱导的松弛无影响。松弛是温度敏感的。前列腺素合成的抑制剂(吲哚美辛和阿司匹林)和沙拉菌素可减弱前列腺素E_1和E_2的松弛作用，花生四烯酸可使去甲肾上腺素收缩的肾静脉条松弛；吲哚美辛可阻断花生四烯酸的松弛作用。这些结果提示：(1)All刺激静脉平滑肌合成前列腺素；(2)内源性前列腺素调节静脉平滑肌对AIL的反应。
The effects of angiotensin II (All) on contractile tension were studied in vascular smooth muscle from dogs, pigs and rabbits. Helically cut strips of renal veins were mounted in organ chambers and isometric contractions were recorded. Contraction of the venous strips was induced by application of 10–8g/ml norepinephrine (NE). Subsequent addition of 5 × 10-8g/ml All caused a triphasic response: (1) there was an initial contraction (subsequent contractions were tachyphylactic in all species); (2) the contraction was followed by a relaxation below the contraction induced by NE (subsequent relaxation responses were tachyphylactic in dog and pig veins), and (3) there was a return from the relaxation to the level of the NE-induced contraction. The duration of the entire response was approximately 5 min. The magnitude of the relaxation varied inversely with the level of the NE contraction when the contractile state was altered by changing the NE concentration. Conditions which inhibit the sodium pump (potassium-free solution and ouabain) and beta-adrenergic blockade with pro-pranolol had no effect on the All-induced relaxation. The relaxation was temperature sensitive. Inhibitors of prostaglandin synthesis (indomethacin and aspirin) and saralasin attenuated the relaxation in response to AIL Prostaglandins E1and E2and arachidonic acid caused relaxation of renal vein strips contracted with NE; the relaxant effect of arachidonic acid was blocked by indomethacin. These results suggest that: (1) All stimulates the synthesis of prostaglandins in isolated venous smooth muscle, and (2) endogenous prostaglandins modulate the response of venous smooth muscle to AIL