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AT1-AA Infusion during Pregnancy Impairs CBF Autoregulation Postpartum
Nathan Campbell1, Luke Strong1, Xing Fang1
1Department of Pharmacology & Toxicology, University of Mississippi Medical Center, Jackson, MS, USA.
Summary
Autoantibodies to the angiotensin II type 1 receptor (AT1-AA) during pregnancy impair cerebral blood flow (CBF) autoregulation postpartum. This impairment persists long-term, suggesting AT1-AA contributes to cerebrovascular issues in preeclampsia survivors.
Area of Science:
- Obstetrics and Gynecology
- Cardiovascular Physiology
- Immunology
Background:
- Preeclampsia (PE) is a significant cause of maternal and fetal morbidity.
- Activated B cells in PE produce autoantibodies to the angiotensin II type 1 receptor (AT1-AA).
- AT1-AA is known to impair cerebral blood flow (CBF) autoregulation during pregnancy, with elevated levels persisting postpartum.
Purpose of the Study:
- To investigate if elevated AT1-AA during pregnancy impairs CBF autoregulation postpartum.
- To determine if a postpartum infusion of AT1-AA further affects CBF autoregulation.
Main Methods:
- Timed-pregnant Sprague Dawley rats received AT1-AA infusions starting gestational day 14.
- Uterine artery resistance index (UARI) measured gestational day 18; mean arterial pressure (MAP) and CBF autoregulation assessed postpartum.
- A subset of dams received a second AT1-AA infusion at 9 weeks postpartum.
Main Results:
- AT1-AA during pregnancy increased UARI, indicating endothelial dysfunction.
- Postpartum CBF autoregulation was impaired in dams exposed to AT1-AA during pregnancy, independent of MAP.
- Postpartum AT1-AA infusion elevated blood pressure but did not worsen CBF autoregulation impairment.
Conclusions:
- Circulating AT1-AA during pregnancy leads to lasting impairment of CBF autoregulation postpartum.
- Elevated AT1-AA may cause long-term cerebrovascular consequences in preeclampsia.
- Targeting AT1-AA could potentially prevent postpartum cerebrovascular complications of preeclampsia.

