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Articles in PresS, published online ahead of print May 30, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00736.2001
Submitted on December 10, 2001
Accepted on May 24, 2002
1 Department of Physiology, University of Adelaide, Adelaide, South Australia, Australia
* To whom correspondence should be addressed. E-mail: caroline.mcmillen{at}adelaide.edu.au.
It has been proposed that fetal adaptations to intrauterine nutrient deprivation permanently reprogram the cardiovascular system. We have investigated the impact of restricted periconceptional nutrition and/or restricted gestational nutrition on fetal arterial blood pressure (BP), heart rate, rate pressure product and the fetal BP responses to angiotensin II and the angiotensin converting enzyme inhibitor, captopril, during late gestation. Restricted periconceptional nutrition resulted in an increase in fetal mean arterial BP between 115-125d gestation (Restricted 41.5 ± 2.8 mmHg, n=12; Control 38.5 ± 1.5 mmHg, n=13) and between 135-147d gestation (Restricted 50.5 ± 2.2 mmHg, n=8; Control 42.5 ± 1.9 mmHg, n=10) as well as an increase in the rate pressure product in twin, but not singleton, fetuses between 115 and 147d gestation . Mean BP and fetal plasma ACTH were also positively correlated in twin, but not singleton fetuses. This is the first demonstration that maternal undernutrition during the periconceptional period results in an increase in fetal arterial BP. This increase occurs concomitantly with an increase in fetal ACTH, but is not dependent on activation of the fetal RAS.
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