title: Systemic vascular reactivity in an aortic coarctation model of preeclampsia in the rat.
abstract: Preeclampsia (preECL), a hypertensive disorder of pregnancy, which occurs only in humans, is dangerous for mother and fetus. It may be caused by placental hypoxia triggering the release of a circulating factor that damages the maternal endothelium leading to vasoconstriction and hypertension. Our primary objective was to determine if systemic vascular reactivity is altered in a rat aortic coarctation (ACOR) model of preECL. We hypothesized that reduced blood flow to the rat utero-placental unit would lead to increased responsiveness to vasoconstrictors. On day 8 of pregnancy, rats were anesthetized and subjected to sham (SHAM) or aortic coarctation (ACOR) surgery by placing a 0.4 mm diameter silver clip distal to the renal arteries. Systemic pressor responses to bolus doses of phenylephrine (PE), angiotensin II (AII), and 5-hydroxytryptamine (5-HT) were determined in these animals on gestation days 14-15 (mid-pregnancy) or 19-20 (late pregnancy). Virgin rats were subjected to sham or ACOR surgery and arterial pressure measured 10-11 days after surgery. Arterial pressure was elevated in late pregnant ACOR animals (mean of 120+/-4 mmHg) compared with SHAM (mean of 101+/-6), but mid-pregnant and virgin groups were not different. Proteinuria was present more frequently in late pregnant ACOR animals (86%) than in SHAM (41%), but there were no differences in average fetal weight, fetal number, or number of reabsorbed fetuses. Pressor responses were not different in ACOR and SHAM groups in mid- or late pregnancy. These data indicate that the aortic coarctation to 0.4 mm in the rat mimics the clinical presentation of mild preECL in humans.
authors.affiliation: Department of Physiology and Biophysics, Health Sciences Center, University of Louisville, 40292, Louisville, KY, USA
authors.forename: M Kristina
authors.initials: MK
authors.lastname: Henzel
authors.forename: Nancy L.
authors.initials: NL
authors.lastname: Alsip