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Placental and Fetal Growth and Development in Late Rat Gestation Is Dependent on Adrenomedullin¹

^a Departments of Obstetrics & Gynecology, ^b Preventive Medicine and Community Health, ^c Pathology, The University of Texas Medical Branch, Galveston, Texas 77555 ^d Division of Endocrinology, Robert Wood Johnson School of Medicine, New Brunswick, New Jersey 08903-0019

Adrenomedullin is a potent, endogenous vasodilator peptide synthesized and secreted by diverse locations such as adrenal glands, lungs, kidneys, vascular smooth muscle, and endothelium. Homozygous deletion of the adrenomedullin gene is embryonic lethal. We hypothesized that adrenomedullin has an important role in placental and fetal growth and development in rat pregnancy. The current study evaluated maternal systolic blood pressure, litter size, placental and pup weight, pup mortality, and placental pathology in pregnant rats following continuous in utero exposure to an adrenomedullin antagonist. Osmotic minipumps were inserted on Gestational Day 14 to continuously deliver either adrenomedullin, adrenomedullin antagonist, or vehicle control. Systolic blood pressure was recorded daily. Pregnant rats were killed on Gestational Day 15–18, 20, and/or 22 to evaluate placental development and fetal growth. The placentas were graded for the presence of necrosis in the decidua and fetal labyrinth as well as fetal vessel development in the labyrinth. A trend toward increased systolic blood pressure was noted between Gestational Days 17 and 20 in mothers treated with adrenomedullin antagonist, but the difference was not statistically significant. Antagonism of adrenomedullin function during rat pregnancy caused fetal growth restriction, decreased placental size, gross necrosis of placental margins and amniotic membranes, histologically deficient fetal vessel development in the labyrinth, and fetal edema. Adrenomedullin contributes to angiogenesis, functions as a growth factor, and helps regulate vascular tone during rat gestation.

First decision: 20 December 2001.

¹ This work was supported in part by NIH HL58144 and WRHR HD01269.

² Correspondence: Andrea G. Witlin, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1066. FAX: 409 747 1669; agwitlin{at}utmb.edu

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