Nitric oxide synthase and changes in oxidative stress levels in embryonic kidney observed in a rabbit model of intrauterine growth restriction.

Abstract

Objective

To study the effect of uteroplacental circulation restriction on endothelial kidney damage in a fetal rabbit model.

Methods

New Zealand rabbits were subjected to 40-50% of uteroplacental artery ligation at day 25 of pregnancy. After 5 days, surviving fetuses were harvested by cesarean section. The gene and protein expression of selected enzymes associated with nitric oxide production and oxidative stress were analyzed in fetal kidney homogenates.

Results

The placenta weight (6,06 ± 0,27, p < 0,0319) and fetal body (19.90 ± 1.03, p < 0,0001) were significantly reduced in the uteroplacental circulation restriction group. The kidneys from restricted fetuses presented a mild vascular congestion and glomerular capillary congestion, without inflammation or hypertrophy. We found eNOS phosphorylation inhibition (0.23 ± 0.13, p < 0.012) and Arginase-2 (0.29 + 0.14, p < 0.023) protein induction in fetal kidneys of the circulation restriction group. Finally, the kidneys from circulation-restricted fetuses showed increased iNOS mRNA (2.68 + 0.24, p < 0.01) and reduced HO-1 mRNA (23 + 1.3, p < 0.003), with increased ROS (1.69 + 0.09, p < 0.001) and nitrotyrosine-protein (1.74 + 0.28, p < 0.003) levels, without changes in Nox mRNA.

Conclusion

We describe significant deregulation of vascular activity and oxidative damage in kidneys of fetal rabbits that have been exposed to restriction of the uterine circulation.

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