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Evidence that the effect of angiotensin II on bovine oocyte nuclear maturation is mediated by prostaglandins E₂ and F₂

Laboratory of Biotechnology and Animal Reproduction, BioRep, Federal University of Santa Maria, 97105-900 Santa Maria, RS, Brazil

Correspondence should be addressed to P B D Gonçalves who is now at Departamento de Clínica de Grandes Animais, Hospital Veterinário, Universidade Federal de Santa Maria, 97105-900 Santa Maria, RS, Brazil; Email: bayard{at}biorep.ufsm.br

Angiotensin II (AngII) prevents the inhibitory effect of follicular cells on oocyte maturation, but its involvement in LH-induced meiotic resumption remains unknown. The aim of this study was to assess the involvement of AngII in LH-induced meiotic resumption and of prostaglandins (PGs) in the action of AngII. In the experiment I, seven cows were superovulated, intrafollicularly injected with 10 µM saralasin (a competitive AngII antagonist) or saline when the follicles reached a diameter larger than 12 mm, and challenged with a GnRH agonist to induce an LH surge. Fifteen hours after GnRH, the animals were ovariectomized and the oocytes were recovered to determine the stage of meiosis. The oocytes from follicles that received saline were in germinal vesicle (GV) breakdown (30.8%) or metaphase I (MI; 69.2%) stage while those that received saralasin were in the GV stage (100%; P<0.001) 15 h after GnRH agonist. In another experiment, oocytes were co-cultured with follicular hemisections for 15 h to determine whether PGs mediate the effect of AngII on meiotic resumption. Indomethacin (10 µM) inhibited AngII-induced meiotic resumption (13.4 vs 77.5% MI without indomethacin; P<0.001). Furthermore, the GV oocytes progressed to MI at a similar rate when PGE₂, PGF₂ or AngII was present in the co-culture system with follicular cells (PGE₂ 77.4%, PGF₂ 70.0%, and AngII 75.0% MI). In conclusion, our results provide strong evidence that AngII mediates the resumption of meiosis induced by an LH surge in bovine oocytes and that this event is dependent on PGE₂ or PGF₂ produced by follicular cells.