Alterations in vascular smooth muscle mass in the spontaneously hypertensive rat. Role of cellular hypertrophy, hyperploidy, and hyperplasia.
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.
- Copyright © 1982 by American Heart Association