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Increased blood pressure sensitivity to angiotensin II in pregnant rats pretreated with agonistic autoantibodies to the angiotensin II type I receptor
Author(s) -
LaMarca Babbette,
Brewer Justin,
wallace Kedra,
Moseley Janae,
Herse Florian,
Dechend Ralf
Publication year - 2011
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.25.1_supplement.822.13
Agonistic autoantibodies to the angiotensin II (AngII) type I receptor (AT1‐AA) have been proposed to be important links between maternal endothelial cell dysfunction and the development of hypertension during preeclampsia. Although the role of AT1‐AA in pregnancy‐induced hypertension is largely unknown, one theory is that binding of the AT1‐AA to the Ang II type 1 receptor (AT1R) increases blood pressure sensitivity to AngII. We have previously shown that binding of AT1‐AA to the AT1R directly enhances AngII‐induced endothelin‐1 production from vascular endothelial cells. Therefore, this study was designed to determine if chronic AT1‐AA enhances AngII‐induced blood pressure increases during pregnancy. We examined the effect of acute administration of ANGII on blood pressure response in AT1‐AA induced hypertensive rats compared to normal pregnant controls. ANGII (100ng/kg/min) was administered via jugular infusion to NP (n=6) controls and chronic AT1‐AA (1:50, n=10)) infused pregnant rats on day 19 of gestation. Blood pressure increased approximately 30mmHg with acute ANGII infusion in NP rats to 141+/−4 mmHg. Interestingly, blood pressure markedly increased approximately 47mmHg in AT1‐AA infused rats to 168+/−7mmHg with acute ANGII infusion into AT1‐AA induced hypertensive pregnant rats. These data support the hypothesis that AT1‐AA enhances the blood pressure response to ANGII during pregnancy.