Ramsay S G, Kenyon C J, Whyte N, McKay I C, Thomson N C, Lindop G B
Department of Respiratory Medicine, West Glasgow Hospitals University NHS Trust, Glasgow, Scotland, U.K.
Clin Sci (Lond). 2000 Jan;98(1):1-7.
Airway remodelling occurs in chronic asthma. Angiotensin II promotes growth in cardiovascular remodelling. Since the renin-angiotensin system is activated in acute severe asthma, we hypothesized that angiotensin II has a role in airway remodelling. A total of 14 young male Wistar rats were randomly divided into two groups. All received 2-week infusions of bromodeoxyuridine, and the experimental group also received angiotensin II. Blood pressure rose in the angiotensin II-infused group [mean levels: pre-infusion, 134.9 (S.D. 14.7) mmHg; post-infusion, 197.1 (22.5) mmHg], and expression of renin mRNA in the renal juxtaglomerular cells was suppressed in these animals. The proportion of bromodeoxyuridine-positive cell nuclei was no different in the airways of control and angiotensin II-infused animals for smooth muscle [mean bromodeoxyuridine index: control, 8. 6% (S.E.M. 1.1%); angiotensin II, 9.3% (1.1%)], epithelium [control, 16.7% (2.3%); angiotensin II, 16.0% (2.2%)] and adventitia [control, 26.4% (2.2%); angiotensin II, 26.6% (2.4%)]. In the arteries, bromodeoxyuridine indices were higher in the angiotensin II-infused rats [18.4% (2.3%)] than in the control animals [9.4% (2.8%)], but no difference was found in the veins [12% (2.9%) and 11.4% (2.6%) respectively]. Morphometry of the airway wall and mesenteric vasculature was no different in the two groups. Therefore a 2-week infusion of angiotensin II increases blood pressure and DNA synthesis in the mesenteric arteries, but does not cause airway remodelling, in the rat.
气道重塑发生于慢性哮喘。血管紧张素II促进心血管重塑中的生长。由于肾素 - 血管紧张素系统在急性重症哮喘中被激活，我们推测血管紧张素II在气道重塑中起作用。总共14只年轻雄性Wistar大鼠被随机分为两组。所有大鼠均接受为期2周的溴脱氧尿苷输注，实验组还接受血管紧张素II。接受血管紧张素II输注的组血压升高[平均水平：输注前，134.9（标准差14.7）mmHg；输注后，197.1（22.5）mmHg]，并且这些动物肾近球细胞中肾素mRNA的表达受到抑制。在对照组和接受血管紧张素II输注的动物的气道中，溴脱氧尿苷阳性细胞核的比例在平滑肌[平均溴脱氧尿苷指数：对照组，8.6%（标准误1.1%）；血管紧张素II组，9.3%（1.1%）]、上皮[对照组，16.7%（2.3%）；血管紧张素II组，16.0%（2.2%）]和外膜[对照组，26.4%（2.2%）；血管紧张素II组，26.6%（2.4%）]方面没有差异。在动脉中，接受血管紧张素II输注的大鼠的溴脱氧尿苷指数[18.4%（2.3%）]高于对照动物[9.4%（2.8%）]，但在静脉中未发现差异[分别为12%（2.9%）和11.4%（2.6%）]。两组气道壁和肠系膜血管系统的形态计量学没有差异。因此，为期2周的血管紧张素II输注会升高大鼠血压并增加肠系膜动脉中的DNA合成，但不会导致气道重塑。
