| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
RESEARCH |

M Barreta, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
J Oliveira, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
R Ferreira, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
A Antoniazzi, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
B Gasperin, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
L Sandri, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
P Gonçalves, Laboratory of Biotechnology and Animal Reproduction, Federal University of Santa Maria, Santa Maria, Brazil
Correspondence: Paulo Bayard Gonçalves, Email: bayard{at}biorep.ufsm.br
Abstract
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 in the action of AngII. In the first experiment, seven cows were superovulated, intrafollicularly injected with 10 µM of 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 breakdown (30.8%) or metaphase I (MI; 69.2%) stage while those that received saralasin were in the germinal vesicle stage (GV; 100%; P<0.001) 15 hours after GnRH agonist. In another experiment, oocytes were co-cultured with follicular hemisections for 15 hours to determine whether prostaglandins mediate the effect of AngII on meiotic resumption. Indomethacin (10 µM) inhibited AngII-induced meiotic resumption (13.4% MI 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% of 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.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |