Abstract

Intrauterine growth restriction (IUGR) is associated with increased risk of neonatal complications; birth hypoxia; impaired neuronal and kidney development; and stillbirth.New Zealand white pregnant rabbits were used to establish a model of IUGR. Rabbit fetuses with twenty‐five days of gestation (25D) were subjected to severe restriction by 40–50% ligature of uteroplacental vessels. At day 30 (120 hrs after surgery) newborns were obtained by caesarean. After delivery, living newborns were weighed. Kidneys were extracted from 39 fetal rabbits (19 controls and 20 IUGR) and gene expression of genes related with hypertonicity (NFAT5), hypoxia (HIF‐1α), and endothelial activity (Arg2, iNOS and eNOS) were evaluated by qRT‐PCR.Experimental IUGR fetuses were significant smaller than controls (39 vs. 48gr, p<0.05). The qRT‐PCR analysis showed a significant increasing in the NFAT5 (1.7 fold, p<0.05), iNOS (3.4 fold, p<0.05) and Arg2 (6.3 fold, p<0.05) mRNA. On the other hand, a significant reduction of eNOS mRNA level (0.34 fold, p<0.05) was observed. The HIF‐1α did not show changes in its mRNA expression.The selective ligature of uteroplacental vessels in the pregnant rabbit demonstrated an important mRNA dysregulation of essential proteins involved in fetal kidney development and adult kidney maintenance. Fondecyt 1100885 and Fondecyt 1110869.

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