2016
DOI: 10.1161/hypertensionaha.116.07971
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Agonistic Autoantibodies to the Angiotensin II Type 1 Receptor Enhance Angiotensin II–Induced Renal Vascular Sensitivity and Reduce Renal Function During Pregnancy

Abstract: Preeclampsia is a multisystemic disorder that is characterized by new-onset hypertension that usually occurs in the third trimester of pregnancy. 1,2 It is estimated that between 3% and 5% of pregnant women in the United States each year have preeclampsia. Preeclampsia is the leading cause of preterm birth, morbidity, and mortality for the mother and the fetus. 1,2Women with preeclampsia have elevated levels of the angiotensin II type 1 receptor autoantibodies (AT1-AA), oxidative stress, reduced renal function… Show more

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Cited by 49 publications
(62 citation statements)
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“…In contrast, women who develop preeclampsia have an exaggerated pressor response to ang II during pregnancy, an effect that is likely mediated by increased circulating inflammatory cytokines and concomitant increases in circulating AT1-AA 16, 17, 41 . Similarly, previously preeclamptic women demonstrate an augmented presser response to systemic ang II infusion post-partum, suggesting that this augmented sensitivity that arises during pregnancy persists post-partum 23 .…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In contrast, women who develop preeclampsia have an exaggerated pressor response to ang II during pregnancy, an effect that is likely mediated by increased circulating inflammatory cytokines and concomitant increases in circulating AT1-AA 16, 17, 41 . Similarly, previously preeclamptic women demonstrate an augmented presser response to systemic ang II infusion post-partum, suggesting that this augmented sensitivity that arises during pregnancy persists post-partum 23 .…”
Section: Discussionmentioning
confidence: 99%
“…This increased sensitivity to ang II is mediated in part through an increased concentration of agonistic autoantibodies (AT1-AA) to the ang II type I receptor (AT 1 R), and contributes to the sequelae of vascular symptoms experienced during preeclampsia 16, 17 . Similarly, pregnant women with preeclampsia have an exaggerated presser response to ang II 1820 and exhibit elevated AT1-AA 21, 22 .…”
Section: Introductionmentioning
confidence: 99%
“…67 Previous studies reported that agonistic autoantibodies are present in the circulation of women with preeclampsia, and this may further enhance Ang II signaling in this population. 68 Interestingly, women with a history of preeclampsia had augmented microvascular constrictor responses to Ang II, indicating that preeclampsia-associated vascular dysfunction persist postpartum. 69 Phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2), induction of NADPH oxidase, phosphorylation of NF-κB (nuclear factor kappa light chain enhancer of activated B cells), and promoter activation in the nucleus have been all implicated in Ang II hypersensitivity in preeclampsia.…”
Section: Angiotensin IImentioning
confidence: 99%
“…When transgenic mice expressing human angiotensinogen are fertilized with transgenic males expressing human renin (with the consequent placenta also expressing human renin), a preeclamptic phenotype is seen [28]. Although the clinical significance is poorly understood, some preeclamptic women display activating autoantibodies directed against ATR1, which is capable of inducing its heterodimerization with the bradykinin b2-receptor and which results in an increased response to AngII (despite lower levels in preeclamptic patients) [29,30]. A state of relative vasodilation is another potential mechanism for the loss of resistance to vasopressors, particularly to AngII, observed in preeclampsia compared with normal pregnancy [31].…”
Section: P R E E C L a M P S I A : F R O M P L A C E N T A D Y S F U mentioning
confidence: 99%
“…Conversely, pregnant women exhibit increased activation of eNOS (through increased phosphorylation); this advantage is lost, however, at the very beginning of preeclampsia [19,36]. Increased production by preeclamptic placentas of soluble endoglin (sENG), the soluble form of the endothelial receptor of transforming growth factor beta (TGF-b), is involved in reduced eNOS activity [29]. By trapping TGF-b and VEGF, sENG and sFlt-1, respectively, thus both contribute to impaired eNOS phosphorylation.…”
Section: P R E E C L a M P S I A : F R O M P L A C E N T A D Y S F U mentioning
confidence: 99%