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Pregnancy-Induced Alterations of Vascular Function in Mouse Mesenteric and Uterine Arteries¹

^a Perinatal Research Centre, Departments of Obstetrics/Gynecology and Physiology, University of Alberta, Edmonton, Alberta, Canada T6G 252

Normal pregnancy involves dramatic changes to maternal vascular function, while abnormal vascular adaptations may contribute to pregnancy-associated diseases such as preeclampsia. Many genetic mouse models have recently emerged to study vascular pathologies of pregnancy. However, vascular adaptations to pregnancy in normal mice are not fully understood. Thus, we studied changes in vascular reactivity during normal mouse pregnancy. We hypothesized that pregnant mice will have enhanced endothelial-dependent vasodilation compared with nonpregnant mice, via an enhancement of the nitric oxide synthase (NOS) prostaglandin H synthase (PGHS), and other endothelial-derived hyperpolarizing pathways. Late pregnant (Day 17–18) C57BL/6J mice (n = 10) were compared with nonpregnant mice (n = 7). Uterine and mesenteric arteries were mounted on a wire myograph system and assessed for endothelium-dependent (methacholine) and -independent (sodium nitroprusside; SNP) relaxation responses. Endothelial-dependent relaxation was enhanced in pregnant uterine and mesenteric arteries, which was blunted after the addition of inhibitors of the PGHS or NOS pathways. In nonpregnant mice, these pathways had no effect in modulating relaxation in uterine arteries, whereas vasodilation in mesenteric arteries was reduced only by NOS inhibition. Both uterine and mesenteric vessels had nonnitric oxide- and nonprostaglandin-mediated relaxation, but this relaxation was not enhanced during pregnancy. Endothelial-independent relaxation was also enhanced in pregnant uterine but not mesenteric arteries. Our data indicate that uterine and mesenteric arteries from pregnant mice have enhanced vasodilation. Understanding vascular adaptations to normal mouse pregnancy is crucial for interpreting changes that may occur in genetic mouse models.

¹ The research was supported by grants from the Canadian Institute of Health Research (CIHR) and the Heart and Stroke Foundation of Alberta, North West Territories, and Nunavut. C.M.C. is supported by a graduate studentship from CIHR and from the Alberta Heritage Foundation for Medical Research (AHFMR). S.T.D. receives salary support from CIHR and AHFMR.

² Correspondence: Sandra T. Davidge, Perinatal Research Centre, 232 HMRC, Departments of Ob/Gyn and Physiology, University of Alberta, Edmonton, AB, Canada T6G 2S2. FAX: 780 492 1308; e-mail: sandra.davidge{at}ualberta.ca