Jrl. De Mola et al., Gonadotropins induce higher active renin levels in the follicular fluid ofnormal and hyperstimulated cycles, GYNECOL END, 13(3), 1999, pp. 155-160
The objective of this study was to analyse follicular fluid active renin;an
d its relationship to steroid hormones throughout the normal and gonadotrop
in-stimulated menstrual cycle. Active renin was measured in the follicular
fluid of patients undergoing tubal sterilization (n = 16) and in vitro fert
ilization (IVF) (n = 25); IVF patients were either in a natural cycle (n;=
7) or undergoing controlled ovarian hyperstimulation (n = 18). The largest
visible follicle was aspirated at the time of laparoscopic tubal sterilizat
ion; ultrasound guided transvaginal follicular aspiration was used in the I
VF group. Follicular fluid active renin, estradiol and progesterone levels
were measured with immunoradiometric and fluoroimmunoassays. The cycle day
was correlated with the spontaneous luteinizing hormone (LH) surge or human
chorionic gonadotropin (hCG) administration, as well as active renin, estr
adiol, progesterone levels and the estradiol/ progesterone ratio using simp
le and multiple regression and analysis of variance (ANOVA). Cycle day inde
pendently influenced active renin, progesterone and the estradiol/progester
one ratio in a statistically significant manner (p < 0.0001). The active ve
nin and progesterone levels were highest during the periovulatory period (p
< 0.0001 and p < 0.002, respectively) and the estradiol/progesterone ratio
correlated inversely with cycle day (p < 0.003). Although the follicular f
luid active venin, estradiol and progesterone levels were higher after cont
rolled ovarian hyperstimulation when compared to natural cycles, this diffe
rence did not reach statistical significance. Our findings suggest that act
ive renin levels in follicular fluid increase in the follicular phase of th
e menstrual cycle, reaching peak levels in the periovulatory period followi
ng the LH surge or hCG administration, providing indirect support for the h
ypothesis that the ovarian renin-angiotensin system (RAS) is under gonadotr
opin control.