Arterial wall hyperplasia is increased in placental compared with myoendometrial radial uterine arteries from late-pregnant rats

Abstract

This study compared myoendometrial versus placental radial uterine arteries from late-pregnant rats to evaluate differences in passive mechanical properties and arterial wall hyperplasia. Myoendometrial and placental radial uterine arteries were dissected from late-pregnant (day 17-19) Sprague-Dawley rats (n = 21) for determination of the lumen diameter and passive distensibility. Arterial wall hyperplasia was evaluated by bromodeoxyuridine incorporation and histologic determination of mitotic indices of endothelial, smooth muscle, and adventitial cells. Nonpregnant radial uterine and mesenteric arteries were used as control cells. Both placental and myoendometrial uterine arteries were significantly larger than nonpregnant uterine arteries by 40% and 28%, respectively (P < .05). The lumen diameter of placental arteries was significantly (16%) larger than adjacent myoendometrial arteries (P < .05). In addition to the larger luminal diameter, placental arteries were significantly more distensible than myoendometrial arteries at all pressures that were studied, which demonstrates differential remodeling. Comparison of mitotic indices revealed that placental arteries had significantly increased cell division rates of both endothelial and smooth muscle significantly compared to myoendometrial arteries. Both types of arteries from pregnant animals had increased cell division rates compared with vessels from nonpregnant animals. The mitotic index of endothelial and smooth muscle cells for placental and myoendometrial arteries from late-pregnant and nonpregnant animals was 15.08% +/- 2.05% and 6.57% +/- 1.37%, 8.73% +/- 1.23%, and 3.04% +/- 0.48% (P < .05 vs placental), and 0.29% +/- 0.29% and 0.23% +/- 0.23% (P < .05 vs placental endothelial), respectively. Adventitial cell division was 10- to 15-fold higher in late-pregnant versus nonpregnant animals. These data demonstrate differential growth and remodeling of uterine arteries that supply the placenta versus the myoendometrium, which likely is facilitated by enhanced arterial wall hyperplasia in placental arteries.