Role of reactive oxygen species in hypertension produced by reduced uterine perfusion in pregnant rats

Mona Sedeek, Jeffrey S. Gilbert, Babbette B. Lamarca, Myssara Sholook, Derrick L. Chandler, Yuping Wang, Joey P. Granger

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99 Scopus citations


Background: Although recent studies indicate preeclampsia (PE) is associated with increased oxidative stress, the role of reactive oxygen species in the hypertension associated with PE remains unclear. We sought to test the hypothesis that placental ischemia increases oxidative stress which in turn, contributes to hypertension. Methods: Reduction in uterine perfusion pressure (RUPP) was induced by placing silver clips on the abdominal aorta and the ovarian arteries on day 14 of pregnancy. On day 20 of pregnancy, mean arterial pressure (MAP) was measured and oxidative stress was assessed in renal and placental tissues whereas systemic administration of tempol, a superoxide dismutase (SOD) mimetic, was used to evaluate the contribution of reactive oxygen species on RUPP-induced hypertension. Results: MAP (120 ± 2 mm Hg vs.106 ± 3 mm Hg), placental levels of 8-isoprostane (1.9 ± 0.4 ng/g tissue vs. 0.8 ± 0.1 ng/g tissue), and malondialdehyde (MDA) (6.9 ± 0.6 μmol/g tissue vs. 3.9 ± 0.4 μmol/g tissue) were increased, whereas renal cortical SOD activity was decreased in RUPP rats (1.2 ± 0.1 units/mg protein vs. 1.6 ± 0.1 units/mg protein) at day 20 of gestation (20 dG) compared to controls. Chronic treatment with tempol attenuated the hypertension (RUPP + tempol 112 ± 2 mm Hg vs. RUPP, 120 ± 2 mm Hg) associated with RUPP, whereas tempol had no effect on MAP (NP, 106 ± 3 vs. NP + tempol, 108 ± 2) in control rats. Conclusion: The results of this study indicate that placental ischemia decreases innate antioxidant activity resulting in elevated oxidative stress which appears to play a role in mediating hypertension associated with chronic RUPP in pregnant rats.

Original languageEnglish (US)
Pages (from-to)1152-1156
Number of pages5
JournalAmerican journal of hypertension
Issue number10
StatePublished - Oct 2008
Externally publishedYes

Bibliographical note

Funding Information:
Acknowledgments:this work was supported by National Institutes of Health (NIH) grants HL-38499 and L-51971.


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