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自发性高血压大鼠血管平滑肌质量的改变。细胞肥大、超倍体和增生的作用。

Alterations in vascular smooth muscle mass in the spontaneously hypertensive rat. Role of cellular hypertrophy, hyperploidy, and hyperplasia.

作者信息

Owens G K, Schwartz S M

出版信息

Circ Res. 1982 Sep;51(3):280-9. doi: 10.1161/01.res.51.3.280.

DOI:10.1161/01.res.51.3.280
PMID:7116579
Abstract

In a previous brief report we demonstrated that differences in aortic smooth muscle mass between spontaneously hypertensive and Wistar-Kyoto rats were due to smooth muscle cell hypertrophy, without hyperplasia. Smooth muscle cell hypertrophy, however, was accompanied by an increase in the frequency of polyploid cells. This study reports (1) the relationship between changes in smooth muscle cell mass and DNA ploidy, (2) the proportion of the increase in mass of smooth muscle in spontaneously hypertensive rats that can be accounted for by polyploid cells, and (3) the time-course of changes in ploidy during the development of hypertension. Flow microfluorimetric and Feulgen-DNA microspectrophotometric measurements demonstrated that the frequency of polyploid smooth muscle cells was 2-3 times greater in spontaneously hypertensive rats than in Wistar-Kyoto rats at 3 months of age and older. The frequency of polyploid cells increased with age and level of blood pressure. No differences in the frequency of polyploid cells were apparent between prehypertensive 1-month spontaneously hypertensive and Wistar-Kyoto rats. By cytospectrophotometric analysis, spontaneously hypertensive rat diploid, tetraploid, and octaploid smooth muscle cells had 36%, 136%, and 377%, respectively, the protein content of Wistar-Kyoto rat diploid cells. The increase in mean cellular protein (53% by cystospectrophotometry) in spontaneously hypertensive rats could account for the total increase (56%) in aortic smooth muscle mass, measured by morphometry. Thus, smooth muscle cell hypertrophy alone can account for the increased mass of smooth muscle in spontaneously hypertensive rat aortas, while the majority of change in smooth muscle mass is due to the increased frequency and mass of polyploid cells.

摘要

在之前的一篇简短报告中,我们证明了自发性高血压大鼠和Wistar - Kyoto大鼠之间主动脉平滑肌质量的差异是由于平滑肌细胞肥大,而非增生。然而,平滑肌细胞肥大伴随着多倍体细胞频率的增加。本研究报告了(1)平滑肌细胞质量变化与DNA倍性之间的关系,(2)自发性高血压大鼠中多倍体细胞可解释的平滑肌质量增加比例,以及(3)高血压发展过程中倍性变化的时间进程。流式微荧光测定法和福尔根DNA显微分光光度测定法表明,3月龄及以上的自发性高血压大鼠中多倍体平滑肌细胞的频率比Wistar - Kyoto大鼠高2 - 3倍。多倍体细胞的频率随年龄和血压水平增加。1月龄的高血压前期自发性高血压大鼠和Wistar - Kyoto大鼠之间多倍体细胞频率无明显差异。通过细胞分光光度分析,自发性高血压大鼠的二倍体、四倍体和八倍体平滑肌细胞的蛋白质含量分别为Wistar - Kyoto大鼠二倍体细胞的36%、136%和377%。自发性高血压大鼠平均细胞蛋白质的增加(通过细胞分光光度法测定为53%)可解释通过形态测量法测得的主动脉平滑肌质量的总增加(56%)。因此,仅平滑肌细胞肥大就可以解释自发性高血压大鼠主动脉中平滑肌质量的增加,而平滑肌质量的大部分变化是由于多倍体细胞的频率和质量增加所致。

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Alterations in vascular smooth muscle mass in the spontaneously hypertensive rat. Role of cellular hypertrophy, hyperploidy, and hyperplasia.自发性高血压大鼠血管平滑肌质量的改变。细胞肥大、超倍体和增生的作用。
Circ Res. 1982 Sep;51(3):280-9. doi: 10.1161/01.res.51.3.280.
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