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Role of Endogenous Angiotensin‐(1‐7) in the Regulation of Prostaglandin Synthetic Enzymes in the Uteroplacental Unit in Late Gestation
Author(s) -
Bharadwaj Manish S,
Brosnihan K. Bridget
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.lb540
Subject(s) - angiotensin ii , prostaglandin , cyclooxygenase , placenta , thromboxane a2 , prostaglandin h2 , medicine , endocrinology , endogeny , fetus , thromboxane , receptor , enzyme , chemistry , andrology , biology , biochemistry , pregnancy , genetics , platelet
Cyclo‐oxygenase (COX) derived prostanoids (PG) regulate numerous maternal/fetal interactions during pregnancy and have been implicated in several pregnancy disorders. Previous studies from our lab have identified the presence of Ang‐(1‐7) and its processing enzyme, ACE2, in the fetal membrane (FM), uterus (U) and placenta (Pl) during late (L) gestation (G) in pregnant (Pr) rats. The objective of this study was to determine the contribution of endogenous Ang‐(1‐7) on the regulation of PG synthetic enzymes during LG. Pr SD rats at day 11 of G were implanted with a mini‐osmotic pump for the intravenous delivery of D‐(Ala)‐Angiotensin‐(1‐7) [D‐Ala], a specific receptor antagonist for Ang‐(1‐7), for 8 days. On day 19 of G, rats were sacrificed by decapitation and FM, Pl, and U tissues were quickly snap‐frozen on dry‐ice. COX‐1 and 2, PGI synthase (syn) [PGIS], PGE syn (PGES), and thromboxane syn (TXAS) were measured with Western blot hybridization. D‐Ala treatment reduced COX‐1, COX‐2, PGIS, PGES, and TXAS in FM; up‐regulated COX‐1 and down‐regulated TXAS in the PL; and up‐regulated COX‐1 and down‐regulated COX‐2 and PGES in the U. In conclusion, endogenous Ang‐(1‐7) exerts a positive regulation on COX‐2 in FM and U in association with a specific up‐regulation of PGES, most likely increasing the production of PGE2. In the Pl, on the other hand, Ang‐(1‐7) up‐regulates TXAS. This research was supported by NHLBI PO1‐HL051952.