Gonadotropins and gonadal steroids play essential roles in the ovarian function. Several factors, including growth factors and regulatory peptides, have also been involved in this function. Recently, natriuretic peptides and the renin-angiotensin system (RAS) have been shown to participate in this process. Local RAS has been described in several organs including the ovaries. All the components of the RAS have been identified in the ovaries: angiotensinogen, angiotensin-I (Ang-I), angiotensin-II (Ang-II), renin, angiotensin-converting enzyme (ACE), and AT1 and AT2 receptors. Ang-II stimulates ovulation, maturation of oocytes, and production of estradiol, progesterone and prostaglandins. HCG stimulates the ovarian production of Ang-II. The inhibition of Ang-II production by ACE inhibition, however, does not change steroidogenesis and ovulation. Such effects could be due to Angiotensin-(1-7), a recently described RAS peptide, which can be formed by an ACE independent pathway. Preliminary results show that Ang-(1-7) induces estradiol release in rat ovary perfused in vitro. Finally, there is evidence that the RAS participates in ovarian disorders such as ovarian hyperstimulation syndrome (OHSS) and polycystic ovary syndrome (PCOS). In OHSS gonadotropin treatment stimulates the ovarian RAS; ACE inhibition decrease the incidence and severity of the syndrome. In PCOS, it has been shown that ovarian renin and Ang-II are increased. The increase of androgen concentration, a basic characteristic of this syndrome, is correlated with the increase of plasma prorenin. Thus, the RAS seems to play an important role in ovarian physiology and pathophysiology.
Ovaries; Gonadal steroids; Renin-angiotensin system; Angiotensins
