American journal of perinatology · 2014
The role of the reduction of spiral artery remodeling and heme oxygenase 1 in mediating AT1-AA-induced hypertension and intrauterine growth restriction in pregnant rats.
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Zhang Dan, Wang Leilei, Qiao Chong, Yu Yang, Fu Lihua, Shang Tao
Аннотация
INTRODUCTION: Recently, emerging evidence has indicated that preeclamptic women who have angiotensin receptor agonistic autoantibodies (AT1-AA), these antibodies contribute to features of the disease.
AIM: The purpose of this study was to determine the role of spiral artery remodeling in mediating AT1-AA-induced hypertension and intrauterine growth restriction in pregnant rats. We hypothesized that AT1-AA-mediated heme oxygenase 1 (HO-1) reduction contributes to decreased spiral artery remodeling. Rat AT1-AA and an HO-1 inducer were administered to pregnant rats.
RESULT: Mean arterial pressure (MAP) increased from 98 ± 4 mm Hg in normal pregnant rats to 113 ± 6 mm Hg in AT1-AA-infused rats (p < 0.05), which was significantly attenuated by the HO-1 inducer (103 ± 2 mm Hg). Fetal weight was also attenuated by HO-1 inducer, and kidney and liver development was adversely affected. Spiral artery remodeling was significantly reduced in AT1-AA-treated pregnant rats compared with that in normal pregnant rats, and this was significantly ameliorated by an HO-1 inducer.
CONCLUSION: Our findings demonstrate that AT1-AA-mediated HO-1 reduction contributes to reduced spiral artery remodeling, and is one mechanism whereby AT1-AA mediates hypertension and intrauterine growth retardation.
AIM: The purpose of this study was to determine the role of spiral artery remodeling in mediating AT1-AA-induced hypertension and intrauterine growth restriction in pregnant rats. We hypothesized that AT1-AA-mediated heme oxygenase 1 (HO-1) reduction contributes to decreased spiral artery remodeling. Rat AT1-AA and an HO-1 inducer were administered to pregnant rats.
RESULT: Mean arterial pressure (MAP) increased from 98 ± 4 mm Hg in normal pregnant rats to 113 ± 6 mm Hg in AT1-AA-infused rats (p < 0.05), which was significantly attenuated by the HO-1 inducer (103 ± 2 mm Hg). Fetal weight was also attenuated by HO-1 inducer, and kidney and liver development was adversely affected. Spiral artery remodeling was significantly reduced in AT1-AA-treated pregnant rats compared with that in normal pregnant rats, and this was significantly ameliorated by an HO-1 inducer.
CONCLUSION: Our findings demonstrate that AT1-AA-mediated HO-1 reduction contributes to reduced spiral artery remodeling, and is one mechanism whereby AT1-AA mediates hypertension and intrauterine growth retardation.