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Endothelial dysfunction after hypertensive pregnancy in the rat
Author(s) -
Colson Drew,
Verzwyvelt Joseph D,
Arany Marietta,
Ojeda Norma,
Gilbert Jeffrey S
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.969.8
Subject(s) - endothelial dysfunction , preeclampsia , medicine , ischemia , sodium nitroprusside , blood pressure , endocrinology , electrical impedance myography , perfusion , pregnancy , endothelium , cardiology , vasodilation , nitric oxide , biology , genetics
Recent evidence indicates formerly preeclamptic women have endothelial dysfunction and increased risk for cardiovascular and renal disease in later life. Despite these observations it remains unclear if these sequelae are due to persistent effects of placental ischemia or are related to underlying genetic or environmental factors associated with preeclampsia. To this end, we employed our model of hypertension associated with reduced uterine perfusion pressure (RUPP) to determine if placental ischemia is associated with persistent changes in vascular function independent of other risk factors. We hypothesized that formerly hypertensive rats with placental ischemia during pregnancy would have endothelial dysfunction four months post‐partum (RUPP‐PP) when compared to normal pregnant post‐partum dams (NP‐PP). Arterial pressure (115 ± 6 vs. 113 ± 5 mmHg) and body weight (272 ± 7 vs. 270 ± 5 g) were not different between NP‐PP and RUPP‐PP groups. Wire myography revealed that endothelial dependent relaxation to ACh was impaired in the RUPP‐PP vs. NP‐PP as evidenced by a rightward shift in the concentration response curve (‐log EC 50 ‐6.0 ± 0.3 vs. ‐6.8 ± 0.2; P <0.05). Smooth muscle dependent relaxation to sodium nitroprusside was unchanged between groups. The present data indicate that vascular endothelial dysfunction is a persistent effect of placental ischemia independent of other cardiovascular risk factors.