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The data suggest that a compromised mechanism of antioxidant defense and an increase in oxidative damage contribute to the development of hypertension and associated vascular dysfunction in 2K-1C rats, and that tempol and apocynin prevent these effects.

Hypoxia-ischemia (HI) is characterized by a reduced supply of oxygen during pregnancy, which leads to both central nervous system and peripheral injuries in the foetus, resulting in impairment in its development. The purpose of this study was to investigate behavioural changes and systemic oxidative stress in adult animals that have been affected by HI during pregnancy. HI was induced by the occlusion of the maternal uterine artery with aneurysm clamps for a period of 45 min on the 18th gestational day. Animals from the sham group were submitted to same surgical procedure as the HI animals, without occlusion of the maternal uterine artery. The control group consisted of non-manipulated healthy animals. At postnatal day 90, the pups were submitted to behavioural tests followed by blood collection. HI adult animals presented an increase in anxiety behaviour and a lack of habituation compared to both sham and control groups. Oxidative damage, assessed by protein and lipid oxidation in serum, did not differ between HI and sham-operated animals. However, HI animals presented reduced activity of the glutathione peroxidase enzyme and increased formation of nitrite, indicating alterations in the systemic antioxidant repair system. Our results suggest an association among HI, systemic oxidative stress and behavioural alterations.

To investigate the systemic and placental oxidant status as well as vascular function in experimental preeclampsia (PE) induced by nitro-L-arginine methyl ester (L-NAME). Fetal parameters and maternal blood pressure, proteinuria, mesenteric arterial bed (MAB) reactivity, and systemic and placental oxidative stress were compared between four groups: pregnant rats receiving L-NAME (60 mg/kg/day, orally) (P + L-NAME) or vehicle (P) from days 13 to 20 of pregnancy and nonpregnant rats receiving L-NAME (NP + L-NAME) or vehicle (NP) during 7 days. L-NAME administration during pregnancy induced some hallmarks of PE, such as hypertension and proteinuria. The P + L-NAME group presented lower weight gain and placental mass as well as reduced number and weight of live fetuses than P group. The vasodilator effect induced by acetylcholine (ACh) and angiotensin II (Ang II) was lower in the perfused MAB from NP + L-NAME and P + L-NAME than in control groups. Otherwise, the nitroglycerine-induced vasodilation and the phenylephrine- and Ang II-induced vasoconstriction were higher in MAB from NP + L-NAME and P + L-NAME groups than in the respective controls. Systemic and placental oxidative damage, assessed by malondialdehyde and carbonyl levels, was increased and activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were reduced in P + L-NAME and NP + L-NAME groups compared to controls. The present data suggest that the oxidative stress and reduced bioavailability of nitric oxide may contribute to attenuation of vasodilator responses to ACh and Ang II, and hyperreactivity to Ang II in the mesentery of preeclamptic rat, which may contribute to the increased peripheral vascular resistance and BP, as well as intrauterine growth restriction in L-NAME-induced PE.