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Genetic deletion of Angiotensin (1–7) receptor Mas promotes a reduced ovulatory outcome.Knockout (Mas-KO) mice exhibit reduced follicularpool.Mas receptor deletion promotes a lower IGF-1 expression in the ovary.Angiotensin-(1–7) [Ang-(1–7)] is a component of Renin-Angiotensin System (RAS) that acts through activation of the G-protein-coupled receptor Mas. Recent studies highlight Ang-(1–7) as an intermediate of gonadotropin in ovarian physiology. Genetically Mas-deficient mice allow the investigation of Ang-(1–7) in the ovulatory process. Therefore, the present study aimed to analyze the effects of Mas gene deletion on ovulation to confirm our hypothesis that Mas Knockout (Mas-KO) mice exhibit impairment in the ovulatory outcome. First, we evaluated the breeding data from our animal facilities and from a breeding experiment. The ovulation was observed directly from oviducts after a superovulation protocol and in the estrus morning. We also checked the follicular pool and mRNA expression of Insulin-like growth factor-1 (IGF-1) in ovaries to investigate a possible reason underlying the reduced ovulation. Mas-KO mice showed a reduced litter size and decreased spontaneous ovulatory rate. Ovarian stimulation by gonadotropins reversed ovulation outcome in Mas-KO mice. Mas deficiency also promoted a reduced ovarian follicular pool and lower IGF-1 mRNA levels, suggesting that Mas receptor plays a role in the survival of ovarian follicle. The reduction of ovulatory rate highlights the relevance of Ang-(1–7)/Mas axis in female reproduction, probably through a reduction of IGF-1 mRNA levels.