Angiotensin II Signaling Promotes Follicle Growth and Dominance in Cattle

Author:

Ferreira Rogério12,Gasperin Bernardo1,Rovani Monique1,Santos Joabel1,Barreta Marcos1,Bohrer Rodrigo1,Price Christopher2,Bayard Dias Gonçalves Paulo1

Affiliation:

1. Laboratório de Biotecnologia e Reprodução Animal (R.F., B.G., M.R., J.S., M.B., R.B., P.B.D.G.), Universidade Federal de Santa Maria, 97105-900 Santa Maria, Brazil

2. Centre de Recherche en Reproduction Animale (R.F., C.P.), Faculty of Veterinary Medicine, University of Montreal, Saint-Hyacinthe, Quebec, Canada QC J2S 8H5

Abstract

It is generally understood that angiotensin II (AngII) promotes follicle atresia in rats, although recent data suggested that this may not be true in cattle. In this study, we aimed to determine in vivo whether AngII alters follicle development in cattle, using intrafollicular injection of AngII or antagonist into the growing dominant follicle or the second largest subordinate follicle. Injection of saralasin, an AngII antagonist, into the growing dominant follicle inhibited follicular growth, and this inhibitory effect was overcome by systemic FSH supplementation. Injection of AngII into the dominant follicle did not affect follicular growth, whereas injection of AngII into the second largest follicle prevented the expected atresia of this subordinate follicle, and the treated follicle grew at the same rate as the dominant follicle for the next 24 h. Inhibition of AngII action in the dominant follicle decreased estradiol concentrations in follicular fluid and the abundance of mRNA encoding aromatase, 3β-hydroxysteroid dehydrogenase, LH receptor, and cyclinD2 in granulosa cells, with minimal effects on theca cells. The effect of AngII on aromatase mRNA levels was confirmed using an in vitro granulosa cell culture system. In conclusion, these data suggest that AngII signaling promotes follicle growth in cattle and does so by regulating genes involved in estradiol secretion and granulosa cell proliferation and differentiation.

Publisher

The Endocrine Society

Subject

Endocrinology

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