Angiotensin II stimulates increased protein synthesis, not increased DNA synthesis, in intact rat aortic segments, in vitro.
Angiotensin II stimulates increased protein synthesis, not increased DNA synthesis, in intact rat aortic segments, in vitro.
复制标题
在体外，血管紧张素 II 在完整的大鼠主动脉节段中刺激蛋白质合成增加，而不是 DNA 合成增加。
DOI：
10.1159/000158979
复制
发表时间：
1993
影响因子：
1.7
通讯作者：
Owens,GK
中科院分区：
文献类型：
--
作者：
Holycross,BJ;Peach,MJ;Owens,GK
关于血管紧张素II（AngII）是否刺激血管平滑肌细胞（SMC）肥大或增生存在相当大的争议。本研究的目的是确定是否拉伸血管壁或AngII治疗增加蛋白质或DNA的合成在体外完整的主动脉环和血管壁的拉伸是否改变生长反应AngII。将大鼠主动脉环固定在无血清培养基中的钢支架上16 h，并进行0或1.5 g的预加载（即被动拉伸）。给予胎牛血清（13%，FBS）或AngII [1 µM，存在或不存在血管紧张素受体拮抗剂氯沙坦（DuP 753）10 µM]，并测量等长张力发展。在14-16 h时向浴中加入35 S-蛋氨酸（3 µCi/ml），以测量蛋白质合成。被动拉伸没有增加蛋白质合成相比，在无预载条件下安装的血管。AngII和FBS引起了类似的增加，在等长张力的发展，但在FBS处理环的张力发展持续4倍以上，在环与AngII治疗。AngII和FBS分别增加了35%和121%的蛋白质合成，但在0或1.5克被动拉伸的环之间的收缩激动剂诱导的蛋白质合成的程度没有差异。Losartan完全消除AngII诱导的张力发展和蛋白质合成。通过3 H-胸腺嘧啶核苷掺入法测定，血管紧张素Ⅱ和胎牛血清均未刺激主动脉环DNA合成增加。这些结果表明，血管紧张素II刺激肥大，而不是在一个完整的血管完全收缩平滑肌细胞增生。
There is considerable controversy regarding whether angiotensin II (AngII) stimulates hypertrophy or hyperplasia of vascular smooth muscle cells (SMC). The purpose of the present study was to determine whether stretch of the vessel wall or AngII treatment increased protein or DNA synthesis in intact aortic rings in vitro and whether stretch of the vessel wall altered the growth responses to AngII. Rat aortic rings were mounted on steel supports in serum-free medium for 16 h and subjected to 0 or 1.5 g of preload (i.e. passive stretch). Fetal bovine serum (13%, FBS) or AngII [1 µM, in the presence or absence of an angiotensin receptor antagonist, losartan (DuP753) 10 µM] was administered and isometric tension development was measured.35S-methionine (3 µCi/ml) was added to the baths at 14-16 h for measurement of protein synthesis. Passive stretch did not increase protein synthesis as compared to vessels mounted under no-preload conditions. AngII and FBS elicited similar increases in isometric tension development, but tension development in FBS-treated rings was sustained 4 times longer than in rings treated with AngII. AngII and FBS increased protein synthesis by 35 and 121%, respectively, but there was no difference in the extent of contractile agonist-induced protein synthesis between rings subjected to 0 or 1.5 g of passive stretch. Losartan totally abolished AngII-induced tension development and protein synthesis. AngII and FBS did not stimulate increased DNA synthesis in aortic rings, as measured by3H-thymidine incorporation. These results suggest that AngII stimulates hypertrophy rather than hyperplasia of fully contractile SMC in an intact vessel.