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Expression of AT1‐R, AT2‐R and Mas‐R in placental and aortic tissue during normal pregnancy and pregnancy‐induced hypertension in rats
Author(s) -
Anguiano Liliana,
Avila Masiel,
Benitez Jessica,
Lopez Pedro
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.1088.5
Subject(s) - angiotensin ii receptor type 1 , angiotensin ii , placenta , pregnancy , medicine , endocrinology , receptor , abdominal aorta , renin–angiotensin system , pathophysiology , aorta , angiotensin receptor , receptor expression , fetus , blood pressure , biology , genetics
Pregnancy is associated with blunted response to angiotensin II (Ang II). In contrast, there is an increased pressor response to this peptide in pregnancy‐induced hypertension (PIH). The mechanisms involved in these changes have not been elucidated. The aim of this work was to determine if pregnancy‐induced hypertension changes the vascular protein expression of Ang II receptors (AT1, AT2), and Ang 1–7 Mas receptor (Mas‐R) from placenta and thoracic and abdominal aorta segments in rats. We used a subrenal aorctic coarctation (SRAC) model in female Wistar rats as an experimental model of PIH. Tissue samples were homogenized and immunoblotted using Anti‐AT1R, AT2‐R and Anti‐Mas antibody. We found a differential regional expression of both receptors AT1 and AT2 in normal pregnancy, with a higher AT1R expression along the aorta and placenta during pregnancy‐induced hypertension. We also found that Mas‐R is also differentially expressed in healthy aortic tissue, and falls during PIH in both segments, while in the placental tissue from hypertensive rats expression was higher in comparison with healthy pregnant rats. In conclusion, these data suggest that vascular AT1 receptor expression and Mas‐R might have a pathophysiological role in PIH, contributing to Ang II vascular hypersensitivity and lack of dilating response. Supported by SIP‐IPN 20100012 and 20101460 grants.