Evaluation of medial hypertrophy in resistance vessels of spontaneously hypertensive rats.
Evaluation of medial hypertrophy in resistance vessels of spontaneously hypertensive rats.
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DOI：
10.1161/01.hyp.11.2.198
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发表时间：
1988-02
期刊：
影响因子：
8.3
通讯作者：
G. Owens;S. Schwartz;M. McCanna
中科院分区：
文献类型：
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作者：
G. Owens;S. Schwartz;M. McCanna
采用形态计量学、生物化学和免疫学相结合的方法，研究了107~111日龄自发性高血压大鼠(SHR)肠系膜阻力血管中层肥大过程中平滑肌细胞肥大、超倍体和增殖的作用。为便于比较，肠系膜动脉按分支顺序进行分类。I级分支血管为直接进入空肠壁的血管，II~IV级分支为较近端血管；IV级分支血管为肠系膜上动脉分支。通过内侧横截面积和平滑肌含量的形态计量学评价灌流固定血管的中层肥厚。SHR肠系膜阻力大血管(III、IV支)较大血管(I、II支)的内侧横截面积和平滑肌含量较正常血压Wistar-京都大鼠(WKY)显著增加，而I、II小阻力血管(I、II支)无明显变化。用酶法分离肠系膜阻力血管，观察细胞肥大和超倍体情况。在这些制剂中，大约80%的细胞被鉴定为平滑肌细胞，使用的是平滑肌特异性异肌动蛋白抗体。分离细胞的Feulgen-DNA显微密度测定显示，肠系膜阻力血管内存在多倍体细胞，但频率很低，SHR和WKY之间无明显差异。同样，从SHR和WKY血管获得的细胞在细胞蛋白含量或相对平滑肌细胞大小(即面积分布)方面也没有观察到差异。这些结果表明，在SHR较大的肠系膜阻力血管中观察到的中膜平滑肌含量的增加不能用平滑肌肥大和超倍体来解释，这表明SHR一定存在增殖。结果表明，对SHR抵抗血管中膜平滑肌肥大的启动机制的研究，至少在高血压的相对早期，应该集中在检测诱导真正的细胞增殖的因素上，而不是肥大和超倍体。
The role of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in medial hypertrophy of mesenteric resistance vessels of 107- to 111-day-old spontaneously hypertensive rats (SHR) was examined using a combination of morphometric, biochemical, and immunological techniques. Mesenteric arteries were classified on the basis of branching order for comparative purposes. Branch level I vessels were those that directly enter the jejunal wall, while Branches II to IV represented more proximal vessels; Branch IV vessels were those that branch from the superior mesenteric artery. Medial hypertrophy was assessed in perfusion-fixed vessels by morphometric evaluation of medial cross-sectional area and smooth muscle content. Medial cross-sectional area and smooth muscle content were significantly increased in larger (Branches III and IV) but not smaller (Branches I and II) mesenteric resistance vessels of SHR compared with control normotensive Wistar-Kyoto rats (WKY). Smooth muscle cell hypertrophy and hyperploidy were evaluated in isolated cells obtained by enzymatic dissociation of mesenteric resistance vessels. Approximately 80% of the cells in these preparations were identified as smooth muscle cells using a smooth muscle-specific isoactin antibody. Feulgen-DNA microdensitometric evaluation of isolated cells showed that polyploid cells were present in mesenteric resistance vessels but at very low frequencies, and no differences were apparent between SHR and WKY. Likewise, no differences in cellular protein content or relative smooth muscle cell size (i.e., area profile) were observed between cells obtained from SHR and WKY vessels. These results demonstrate that the increase in medial smooth muscle content observed in larger mesenteric resistance vessels of SHR cannot be accounted for by smooth muscle hypertrophy and hyperploidy, inferring that hyperplasia must be present. Results indicate that studies of the initiating mechanisms for medial smooth muscle hypertrophy in SHR resistance vessels, at least relatively early in hypertension, should focus on examination of factors that induce true cellular proliferation rather than hypertrophy and hyperploidy.