Hypertrophic and hyperplastic effects of pregnancy on the rat uterine arterial wall.

OBJECTIVE: The purpose of this study was to characterize the cellular mechanisms (hypertrophy or hyperplasia) contributing to uterine arterial growth during pregnancy. STUDY
DESIGN: Vascular smooth muscle cells were enzymatically dispersed from radial uterine arteries from nonpregnant (n = 4) and late pregnant (day 20 to 21, n = 6) Sprague-Dawley rats, and the axial length was measured. Midpregnant (days 9 to 11, n = 5), late pregnant (n = 5), and nonpregnant (n = 5) Sprague-Dawley rats were injected with bromodeoxyuridine, and immunohistochemistry was used to visualize dividing and nondividing vascular smooth muscle cells and endothelial cells in both radial and main uterine arteries.
RESULTS: Vascular smooth muscle cells isolated from late-pregnant vessels were 21% longer than those from nonpregnant animals, increasing from 118 +/- 4 microns in nonpregnant rats to 150 +/- 7 microns in late-pregnant rats. Cell proliferation rates of both vascular smooth muscle cells and endothelial cells were quite low in nonpregnant animals but increased significantly during pregnancy in both radial and main uterine arteries. The pattern of changes in cell division rates over time, however, varied between the different arterial segments: in midpregnancy rates of both vascular smooth muscle cell and endothelial cell division were highest in the smaller radial arteries, whereas at term the mitotic index values were increased in main uterine arteries.
CONCLUSIONS: Gestational growth of the uterine vasculature is accomplished by a combination of both cellular hypertrophy and hyperplasia in the arterial wall. Furthermore, local differences in cell division rates at different times during gestation suggest the existence of spatially discrete growth mechanisms within the vascular network.