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Poster Session 2

Category: Hypertension

Poster Session 2

(596) Perinatal AT1-AA Exposure is a Risk Factor for Preeclampsia

Wednesday, February 11, 2026

3:30 PM - 5:00 PM

Submitting Author and Presenting Author(s)

Melissa S. Helmich, MD

Maternal Fetal Medicine Fellow
University of Mississippi Medical Center
Jackson, Mississippi, United States

Coauthor(s)

Nathan Campbell, PhD

Instructor
University of Mississippi Medical Center
Jackson, Mississippi, United States
EG

Ella Goolsby

University of Mississippi Medical Center
Jackson, Mississippi, United States
EJ

Emma Grace Joyner

University of Mississippi Medical Center
Jackson, Mississippi, United States
AD

Alexandra Demesa, MS

University of Mississippi Medical Center
Jackson, Mississippi, United States
EL

Evan Lamarca

University of Mississippi Medical Center
Jackson, Mississippi, United States
TT

Ty Turner, BS

University of Mississippi Medical Center
Jackson, Mississippi, United States
BZ

Baoying Zheng, MS

University of Mississippi Medical Center
Jackson, Mississippi, United States
Babbette LaMarca, PhD

Professor and Chair
The University of Mississippi Medical Center
Jackson, Mississippi, United States

Objective:
Preeclampsia (PE) is new-onset hypertension with multi-organ dysfunction during pregnancy. Female children from PE pregnancies are at risk for developing PE during pregnancy, indicating a familial connection. Agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA) are produced in PE women and cause a PE phenotype in pregnant rats. We have shown that perinatal AT1-AA exposure causes adult female offspring to have elevated blood pressure. However, the role of perinatal AT1-AA exposure to increase the risk for a PE phenotype is unknown. Thus, we hypothesize that perinatal AT1-AA exposure will cause female offspring to develop hypertension and fetal growth restriction during pregnancy.

Study Design:
We infused AT1-AA (1:40) from gestational day (GD)14 throughout pregnancy and allowed the dams (F0) to give birth. Birth weight was measured within 12 hours. OS (F1) were aged to 3 months. Control males and females or AT1-AA females were mated. Pregnancy was confirmed by vaginal smear. On GD18 carotid catheters were inserted. On GD19, mean arterial pressure (MAP), weights, and litter sizes were measured. Placental and renal preproendothelin were measured by RT-PCR. Immune cells were measured with flow cytometry. A student’s t-test was used for statistical analysis.

Results:
F1 AT1-AA had increased MAP and smaller litters compared to F1 NP (117±3 mmHg, p< 0.05 vs 105±2 mmHg) (7±2, vs 13±1 pups, p< 0.05). Placental T helper cells were significantly increased in F1 AT1-AA (34±3 % gated) compared to F1 NP (16±3 % gated) with decreased T regulatory cells in F1 AT1-AA (0.44±0.12 % gated) compared to F1 NP (1.27±0.40 % gated). AT1-AA female F1 conceived earlier than normal pregnant (NP) female F1 (14±2 weeks, vs 16±3 weeks, p< 0.05). F1 AT1-AA were smaller at gestational day 19 than F1 NP (293±5g, vs 338±7g, p< 0.0001). Placental PPET and renal PPET were significantly increased 9.5±2.0 fold; 7.5±2.5 fold in F1 AT1-AA compared to F1 NP.

Conclusion:

These data demonstrate that perinatal AT1-AA exposure predisposes F1 females toward PE phenotype thereby contributing to the familial risk for PE.