Vascular smooth muscle cell proliferation in arterioles of the human endometrium.

Menorrhagia affects approximately 15% of all women, often without identifiable cause. Endometrial spiral arterioles are believed to play a major role in controlling menstruation, and are a major site of menstrual loss. We postulate that alterations in the growth and development of spiral arterioles, particularly the vascular smooth muscle cells (VSMC), may contribute to menorrhagia. We examined VSMC proliferation around endometrial arterioles in control and menorrhagic tissues and the possible roles of transforming growth factor beta (TGF-beta) and endothelin in this process. Proliferating VSMC were located immuno-histochemically, then evaluated using computer-aided image analysis. VSMC proliferation was low and constant during the early stages of the menstrual cycle, increasing at the mid to late secretory stages (P < 0.002). Menorrhagic women had significantly reduced VSMC proliferation in their spiral arterioles at the mid and late secretory stages (P < 0.02). VSMC around straight arterioles proliferated at similar rates across the cycle, apart from a significant decrease in VSMC proliferation in menorrhagic women at the late secretory stage (P < 0.002). Endothelin concentrations decreased significantly in the epithelium of menorrhagic women (P = 0.05), while TGF-beta demonstrated no significant differences in the mid to late secretory tissues studied. The results indicate a significant functional difference between the spiral arterioles of control and menorrhagic women that may play a role in menorrhagia, while leaving the roles of endothelin and TGF-beta undetermined.