Owens G K, Schwartz S M, McCanna M
Department of Physiology, University of Virginia, School of Medicine, Charlottesville 22908.
Hypertension. 1988 Feb;11(2):198-207. doi: 10.1161/01.hyp.11.2.198.
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.
采用形态学、生物化学和免疫学技术相结合的方法，研究了107至111日龄自发性高血压大鼠（SHR）肠系膜阻力血管中层肥厚过程中平滑肌细胞肥大、超倍体和增生的作用。为便于比较，根据分支顺序对肠系膜动脉进行分类。I级分支血管是直接进入空肠壁的血管，而II至IV级分支代表更近端的血管；IV级分支血管是从肠系膜上动脉分支出来的血管。通过对灌注固定血管的中层横截面积和平滑肌含量进行形态学评估，来评价中层肥厚情况。与对照正常血压的Wistar-Kyoto大鼠（WKY）相比，SHR较大（III级和IV级分支）而非较小（I级和II级分支）的肠系膜阻力血管的中层横截面积和平滑肌含量显著增加。通过酶解肠系膜阻力血管获得分离细胞，对其进行平滑肌细胞肥大和超倍体评估。使用平滑肌特异性同工肌动蛋白抗体，这些制剂中约80%的细胞被鉴定为平滑肌细胞。对分离细胞进行Feulgen-DNA显微密度测定评估显示，肠系膜阻力血管中存在多倍体细胞，但频率非常低，且SHR和WKY之间无明显差异。同样，从SHR和WKY血管获得的细胞之间，未观察到细胞蛋白含量或相对平滑肌细胞大小（即面积轮廓）的差异。这些结果表明，SHR较大的肠系膜阻力血管中观察到的中层平滑肌含量增加，不能用平滑肌肥大和超倍体来解释，推断必然存在增生。结果表明，对SHR阻力血管中层平滑肌肥大起始机制的研究，至少在高血压相对早期，应侧重于检查诱导真正细胞增殖而非肥大和超倍体的因素。
