Mitogenic effect of angiotensin II on rat carotid arteries and type II or III mesenteric microvessels but not type I mesenteric microvessels is mediated by endogenous basic fibroblast growth factor.
Mitogenic effect of angiotensin II on rat carotid arteries and type II or III mesenteric microvessels but not type I mesenteric microvessels is mediated by endogenous basic fibroblast growth factor.
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DOI：
10.1161/01.res.82.3.321
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发表时间：
1998-02
影响因子：
20.1
通讯作者：
E. Su;D. Lombardi;J. Wiener;M. Daemen;M. Reidy;S. Schwartz
中科院分区：
文献类型：
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作者：
E. Su;D. Lombardi;J. Wiener;M. Daemen;M. Reidy;S. Schwartz
本研究采用抗碱性成纤维细胞生长因子（anti-bFGF）抗体检测血管壁中和bFGF能否阻断血管紧张素II在体内的有丝分裂作用。实验动物分为6个实验组，分别给予(1)血管紧张素II，(2)血管紧张素II +抗bfgf抗体，(3)血管紧张素II +正常山羊IgG (ngIgG),(4)抗bfgf抗体，(5)ngIgG,(6)林格液。血管紧张素II以435 ng x kg(-1) x min（-1）连续输注大鼠1周，诱导平滑肌细胞复制，抗bfgf抗体或ngIgG在1周内静脉注射4次，剂量为60 mg/支。溴脱氧尿嘧啶（30mg /mL）连续输注1周。治疗第4天，所有动物左颈动脉均气球损伤，第7天处死各组研究。结果显示，血管紧张素II显著刺激球囊损伤颈动脉、完整颈动脉和肠系膜血管树三个分支水平的平滑肌复制。抗bfgf能够阻断大血管血管紧张素II的有丝分裂作用，但不能阻断肠系膜动脉树的最小（I型）微血管。这种差异反应可能归因于I型血管病变与大血管病变的性质：I型血管病变具有大量增殖巨噬细胞，而大血管损伤较小，巨噬细胞较少，平滑肌复制水平不同。我们的数据表明，血管紧张素ii处理的大血管的血管壁重塑涉及依赖于bFGF存在的DNA复制。
In this study, anti-basic fibroblast growth factor (anti-bFGF) antibody was used to determine whether the mitogenic effect of angiotensin II in vivo could be blocked by neutralizing bFGF in the vessel wall. Animals, divided into six experimental groups, were given (1) angiotensin II, (2) angiotensin II + anti-bFGF antibody, (3) angiotensin II + normal goat IgG (ngIgG), (4) anti-bFGF antibody, (5) ngIgG, and (6) Ringer's solution. Angiotensin II at 435 ng x kg(-1) x min(-1) was infused into rats continuously for 1 week to induce smooth muscle cell replication, and anti-bFGF antibody or ngIgG was injected intravenously 4 times over the 1-week period at a dose of 60 mg/injection. Bromodeoxyuridine (30 mg/mL) was also continuously infused during the 1-week period. The left carotid artery of all animals was balloon-injured on day 4 of the treatment, and all groups were killed for study on day 7. The results showed that angiotensin II significantly stimulated smooth muscle replication in the balloon-injured carotid artery, intact carotid artery, and three branch levels of the mesenteric vascular tree. Anti-bFGF was able to block the mitogenic effect of angiotensin II in larger vessels but not the smallest (type I) microvessels of the mesenteric arterial tree. This differential response may be attributable to the nature of the lesions in type I vessels versus larger vessels: the type I vascular lesion has a large component of proliferating macrophages, whereas the larger vessels show less injury, few macrophages, and varying levels of smooth muscle replication. Our data suggest that the vessel wall remodeling in the angiotensin II-treated larger vessels involves DNA replication that is dependent on the presence of bFGF.