Background: Hyperandrogenism is a pivotal mediator in the pathogenesis of the polycystic
ovary syndrome (PCOS), but the mechanisms of androgen excess in this condition are not
fully understood. Angiotensin (Ang)-(1-7) is an active peptide of the renin-angiotensin system
(RAS) that stimulates ovarian follicular growth and testosterone release in vitro.
Objective: To investigate whether Ang-(1-7), its receptor Mas and angiotensin-converting enzyme
2 (ACE2), the enzyme that converts Ang II into Ang-(1-7), are expressed in rat polycystic ovaries
(PCO) and thus if this peptide system might be associated with excess androgen production in
Methods: A rat model that shares some features of PCOS such as disruption of folliculogenesis
and multiple ovarian cyst formation was used in the study.
Results: We found reduced levels of Ang-(1-7) and Mas receptor in PCO compared to normal
ovaries. Also, ACE2 mRNA expression was reduced in PCO compared to ovaries of control rats (p
< 0.05). PCO had high levels of estrogen and testosterone and increased mRNA for upstream enzymes
of the steroidogenic cascade, but not of P450 aromatase.
Conclusion: These findings suggest that the ovarian ACE2-Ang-(1-7)-Mas receptor axis is inhibited
and therefore may not be a co-factor of excess testosterone production in rat PCO.