The Role of Maternal Protein Intake During Late Gestation on Placental Vascular Function

• Main Author: Lekatz, Leslie Ann
• Format: Others
• Published: North Dakota State University 2017
• Online Access: https://hdl.handle.net/10365/27116

Global nutrient restriction or excess can influence umbilical hemodynamics in sheep fetuses (Chapter 2). We hypothesized that a specific component of the diet, namely maternal metabolizable protein (MP), would alter placental function. When MP restriction during late gestation occurs, we hypothesized that there would be a decrease in the sensitivity to bradykinin (BK) of the placental vascular arteries. In experiment 1, ewes received one of three isocaloric dietary treatments during late gestation: MP60: 60% of MP requirements; MP80: 80% of MP requirements; and MP100: 100% of the MP requirements on a dry matter basis from day 100 to 130 of gestation. In experiment 1, fetal and placental mass were not affected by dietary treatment; however, placental function was altered by a maternal diet low in protein. Ewes not meeting MP requirements during late gestation had fetal placental arteries that were more sensitive to BK-induced vasorelaxation; therefore we reject our hypothesis for experiment 1. In order to understand the mechanism of BK-induced vasodilation in the placental arteries, experiment 2 was designed. We hypothesized that MP level would alter the mechanism of BK-induced vasorelaxation in placental arteries. In experiment 2, ewes received one of three isocaloric dietary treatments during late gestation: MP60: 60% of MP requirements; MP100: 100% of the MP requirements; and MP140: 140% of MP requirements from day 100 to 130 of gestation. Maternal protein level during gestation did not impact the mechanism of BK-induced vasodilation; therefore we reject our hypothesis for experiment 2. However, the maternal and fetal placental vessels responded to BK through different iv mechanisms. In maternal placental arteries, pathways involving endothelium-derived hyperpolarizing factors (EDHF) and nitric oxide (NO) were responsible for BK-induced vasodilation, while the prostacyclin (PGI2) pathway did not greatly contribute to BKinduced vasodilation. The fetal placental arteries responded to BK through a mechanism that does not involve EDHF, NO, or PGI2, indicating that BK-induced vasorelaxation of the fetal placental arteries may be mediated through an unclassified EDHF-like pathway. It is important to realize the maternal and fetal placental arteries may respond to BKinduced vasodilation through different pathways when considering possible therapeutics for compromised pregnancies.