Simon G, Altman S
Department of Medicine, Veterans Administration Medical Center, Minneapolis, MN 55417.
J Hypertens. 1992 Oct;10(10):1165-71. doi: 10.1097/00004872-199210000-00009.
The proposition that angiotensin II in subpressor does stimulates vascular growth in vivo was tested.
Young adult, male Sprague-Dawley rats received angiotensin II, 200 ng/kg per min intraperitoneally by osmotic minipump, for 24 h or 7-10 days. Sham-infused rats served as controls.
Protein (35S-methionine) synthesis in aortic media, portal vein, bladder wall and diaphragm; proteoglycan (35S-sulfate) synthesis in aorta and bladder and synthesis of DNA (3H-thymidine) in aortic media were all measured ex vivo in the rat.
The systolic blood pressure of angiotensin II-treated rats was unchanged at 24 h and increased at 7-10 days. At 24 h in angiotensin II-treated rats the protein synthesis in aortic media, portal vein and bladder wall but not in the diaphragm was increased, indicating that the hypertrophic effect of angiotensin II was independent of the arterial pressure. The rate of 35S-methionine washout from angiotensin II- and sham-treated aorta was the same. At 24 h there was also an increase in proteoglycans synthesis of the aorta and bladder wall of angiotensin II-treated rats. In contrast to protein synthesis, the incorporation of 3H-thymidine into aortic muscle DNA was reduced in angiotensin II-treated rats at 24 h, suggesting the inhibition of DNA synthesis. At 7-10 days angiotensin II administration the protein synthesis of aortic media returned to baseline, and DNA synthesis was bimodal: in 53% of rats (n = 10) inhibition continued, and in 26% (n = 5) it was increased by two- to threefold.
The present findings confirm in vivo the bifunctionality of the trophic vascular action of angiotensin II. Vascular hypertrophy may play a role in the slow pressor action of angiotensin II.
验证体内亚升压剂量的血管紧张素II是否刺激血管生长这一命题。
成年雄性斯普拉格-道利大鼠通过渗透微型泵以每分钟200 ng/kg的剂量腹腔内注射血管紧张素II，持续24小时或7 - 10天。假注射大鼠作为对照。
在大鼠离体状态下测量主动脉中膜、门静脉、膀胱壁和膈肌的蛋白质（35S - 蛋氨酸）合成；主动脉和膀胱中蛋白聚糖（35S - 硫酸盐）合成以及主动脉中膜DNA（3H - 胸腺嘧啶核苷）合成。
血管紧张素II处理的大鼠收缩压在24小时时未改变，在7 - 10天时升高。在血管紧张素II处理的大鼠中，24小时时主动脉中膜、门静脉和膀胱壁的蛋白质合成增加，但膈肌未增加，这表明血管紧张素II的肥厚作用独立于动脉压。血管紧张素II处理组和假处理组主动脉中35S - 蛋氨酸的洗脱速率相同。24小时时，血管紧张素II处理的大鼠主动脉和膀胱壁的蛋白聚糖合成也增加。与蛋白质合成相反，血管紧张素II处理的大鼠在24小时时主动脉肌DNA中3H - 胸腺嘧啶核苷的掺入减少，提示DNA合成受到抑制。在给予血管紧张素II 7 - 10天时，主动脉中膜的蛋白质合成恢复到基线，DNA合成呈双峰：53%的大鼠（n = 10）持续受到抑制，26%的大鼠（n = 5）增加了2至3倍。
本研究结果在体内证实了血管紧张素II对血管的营养作用具有双重功能。血管肥厚可能在血管紧张素II的缓慢升压作用中起作用。
