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(60) MATERNAL UNDERNUTRITION LEADS TO ADAPTATION OF FETAL VASCULAR REACTIVITY TO ANGIOTENSIN II AND ENDOTHELIN-1 IN PLACENTOMES OF PREGNANT EWES AT MIDGESTATION. Löhle, Matthias1, Kimura, Yoshitaka2, Rhoads, Angela3, Ford, Stephen3, Nathanielsz, Peter1, Nijland, Mark1, 1 New York University, New York, NY2 Tohoku University Graduate School of Medicine, Sendai, Japan3 University of Wyoming, Laramie, WY ABSTRACT- Epidemiological data suggest that under nutrition during pregnancy is a risk factor for adult cardiovascular disease. Animal studies indicate that maternal under nutrition alters fetal cardiovascular function. The investigation of placental vessels in this context is of special interest since the placenta receives a major proportion of the fetal cardiac output and offers the opportunity to examine fetal and maternal vasculature simultaneously. To assess vascular reactivity of placental arteries following maternal under nutrition, pregnant ewes received either 100% (controls, C, n=17) or 50% (nutrient-restricted, NR, n=13) of NRC requirements between 28 and 78 days of gestation (dGA, term 147 days). Half of the NR ewes were re-alimented after 78 dGA. Following necropsy at 78 and 135 dGA, we examined in vitro responsiveness of small fetal and maternal placental arteries ( KEY WORDS: myography, sheep, undernutrition, placenta |
250-700 
m) to potassium chloride (KCL), norepinephrine (NE), angiotensin II (AT II) and endothelin-1 (ET-1) in both ages using wire myography. Whereas there were no treatment differences in the response to KCL and NE, fetal placental arteries of NR animals at 78dGA showed a greater maximum tension generated to AT II (169 ± 22.8% of K+ response, n=7 vs. 100 ± 5.7%, n=6, mean ± SEM, p<0.05) and a diminished maximum tension generated to ET-1 (157 ± 30.0% of K+ response, n=8 vs. 236 ± 20.7%, n=7, p<0.05) compared to vessels from control fetuses. After pre-incubation with L-NAME, the differences in the fetal response to ET-1 decreased with the EC50 in NR fetuses being higher than in C fetuses (p<0.05). However, all changes in vascular reactivity disappeared in fetuses at 135 dGA whose mothers had been re-alimented. There were no treatment differences in the vascular reactivity of maternal placental arteries. Our results suggest that maternal under nutrition from early to mid gestation increases the number of AT II receptors and the ratio of ETB to ETA receptors in fetal placental arteries. While the increased response to AT II in fetal placental arteries might contribute to the elevated systemic blood pressures recently observed in undernourished fetuses at late gestation, the decrease in the responsiveness of fetal placental arteries to ET-1 likely reflects an adaptive mechanism to compensate for nutrient deprivation.