Abstract:The present study was undertaken to assess the role of ovarian renin-angiotensin system (RAS) in the preovulatory cascade induced by gonadotropin exposure. In the in vitro perfused rabbit ovaries, exposure to human chorionic gonadotropin (hCG) enhanced the secretion rate of angiotensin II (Ang II) within 1 h. The secretion rate reached maximal levels at 6 h and then declined thereafter. The intrafollicular Ang II content and renin-like activity were also significantly increased at 2 and 4 h after exposure to h… Show more
“…We demonstrated previously a direct effect of Ang II on the rabbit ovary, suggesting that Ang II may play a critical role in the ovulatory cascade (7,20,30). The addition of saralasin, a peptide Ang II antagonist, to the perfusate blocked hCG-induced ovulation in vitro in a dose-dependent manner (20).…”
The interactions between insulin-like growth factor-I (IGF-I) and the renin-angiotensin system (RAS) in follicular growth and ovulation were studied with the use of an isolated perfused rabbit ovary preparation. Ovulation failed to occur in either control ovaries or the experimental ovaries perfused with IGF-I in a concentration of 1, 10, or 100 ng/ml in the absence of gonadotropin. Exposure to IGF-I stimulated the secretion rate of angiotensin II-like immunoreactivity (Ang II-IR) in perfused rabbit ovaries in a dose-dependent manner. The percent increase in follicle diameter in ovaries perfused with IGF-I for 12 h was significantly correlated with the secretion rate of Ang II-IR at 12 h after exposure to IGF-I. The addition of IGFBP-3 to the perfusate did not induce ovulation in the absence of gonadotropin, but exposure to IGFBP-3 inhibited hCG-induced ovulation in a dosedependent manner. In addition, IGFBP-3 significantly reduced the ovarian secretion rate of Ang II-IR and prostaglandins stimulated by hCG administration. Intrafollicular plasminogen activator (PA) activity significantly increased within 4 h after exposure to 100 ng/ml of IGF-I, compared with that in control ovaries perfused with medium alone. The concomitant addition of IGFBP-3 to the perfusate significantly reduced the IGF-I-stimulated PA activity in the preovulatory follicles at 4, 6, and 8 h after exposure to IGF-I. However, IGFBP-3 alone affected neither the ovarian secretion rate of Ang II-IR nor intrafollicular PA activity. Exposure to streptokinase, an exogenous PA, in vitro stimulated both follicular growth and the intrafollicular Ang II-IR content. In conclusion, IGF-I enhances both ovarian Ang II production and follicular development by stimulating intrafollicular PA activity. ( J. Clin. Invest. 1996. 98:308-316.)
“…We demonstrated previously a direct effect of Ang II on the rabbit ovary, suggesting that Ang II may play a critical role in the ovulatory cascade (7,20,30). The addition of saralasin, a peptide Ang II antagonist, to the perfusate blocked hCG-induced ovulation in vitro in a dose-dependent manner (20).…”
The interactions between insulin-like growth factor-I (IGF-I) and the renin-angiotensin system (RAS) in follicular growth and ovulation were studied with the use of an isolated perfused rabbit ovary preparation. Ovulation failed to occur in either control ovaries or the experimental ovaries perfused with IGF-I in a concentration of 1, 10, or 100 ng/ml in the absence of gonadotropin. Exposure to IGF-I stimulated the secretion rate of angiotensin II-like immunoreactivity (Ang II-IR) in perfused rabbit ovaries in a dose-dependent manner. The percent increase in follicle diameter in ovaries perfused with IGF-I for 12 h was significantly correlated with the secretion rate of Ang II-IR at 12 h after exposure to IGF-I. The addition of IGFBP-3 to the perfusate did not induce ovulation in the absence of gonadotropin, but exposure to IGFBP-3 inhibited hCG-induced ovulation in a dosedependent manner. In addition, IGFBP-3 significantly reduced the ovarian secretion rate of Ang II-IR and prostaglandins stimulated by hCG administration. Intrafollicular plasminogen activator (PA) activity significantly increased within 4 h after exposure to 100 ng/ml of IGF-I, compared with that in control ovaries perfused with medium alone. The concomitant addition of IGFBP-3 to the perfusate significantly reduced the IGF-I-stimulated PA activity in the preovulatory follicles at 4, 6, and 8 h after exposure to IGF-I. However, IGFBP-3 alone affected neither the ovarian secretion rate of Ang II-IR nor intrafollicular PA activity. Exposure to streptokinase, an exogenous PA, in vitro stimulated both follicular growth and the intrafollicular Ang II-IR content. In conclusion, IGF-I enhances both ovarian Ang II production and follicular development by stimulating intrafollicular PA activity. ( J. Clin. Invest. 1996. 98:308-316.)
“…The evidence that supports the existence of an ovarian RAS includes the following: i) the concentrations of Ang II in the follicular fluid were found to be higher than those in the plasma after human chorionic gonadotropin (hCG) treatment (Husain et al 1987), ii) high follicular fluid levels of Ang II were found after bilateral nephrectomy (Husain et al 1987), and iii) in vitro-perfused rabbit ovaries produced Ang II when exposed to hCG (Yoshimura et al 1994). However, renin is produced exclusively by kidneys and disappears from the plasma after bilateral nephrectomy (Do et al 1987).…”
Angiotensin (Ang) II is widely known for its role in the control of systemic blood vessels. Moreover, Ang II acts on the vascular control of ovarian function, corpus luteum formation, and luteolysis. Over the past 10 years, our research group has been studying the new concept of the renin-angiotensin system (RAS) as an autocrine/paracrine factor regulating steroidogenesis and promoting different cellular responses in the ovary, beyond vascular function. We have developed and used different in vivo and in vitro experimental models to study the role of RAS in the ovary and a brief overview of our findings is presented here. It is widely accepted that there are marked species differences in RAS function in follicle development. Examples of species-specific functions of the RAS in the ovary include the involvement of Ang II in the regulation of follicle atresia in rats vs the requirement of this peptide for the dominant follicle development and ovulation in rabbits and cattle. More recently, Ang-(1-7), its receptor, and enzymes for its synthesis (ACE2, NEP, and PEP) were identified in bovine follicles, implying that Ang-(1-7) has an ovarian function. Other novel RAS components (e.g. (pro)renin receptor and renin-binding protein) recently identified in the bovine ovary show that ovarian RAS is poorly understood and more complex than previously thought. In the present review, we have highlighted the progress toward understanding the paracrine and autocrine control of ovarian antral follicle development and ovulation by ovarian tissue RAS, focusing on in vivo studies using cattle as a model.
“…(Rodland et al, 1992 (Werb and Burleigh, 1974) and rat uterus (Woessner and Ryan, 1973 (Zhu and Woessner, 1991) or from compartmentalization of the enzyme to the apex and the inhibitors to different compartments such as the granulosa cell layer (Mann et al, 1991 (Wan et al, 1996), or that there are divergent effects of calcium depending upon the intracellular concentration as previously reported for inositol phosphate (Bezprozvanny et al, 1991). (Pucell et al, 1987(Pucell et al, , 1991 (Kuo et al, 1991;Yoshimura et al, 1992Yoshimura et al, , 1994Yoshimura et al, , 1996bPeterson et al, 1993a). In loto, these findings suggest that All plays a role in follicular rupture.…”
Section: Introductionmentioning
confidence: 55%
“…Similarly, administration of captopril to perfused rabbit ovaries had no effect on ovulatory efficiency (Yoshimura et al, 1994 (Erickson, 1983) …”
\ m=-\ 1 (decrease to 33 \ m=+-\7% and 31 \ m=+-\ 5% of control culture values, respectively). Addition of LH to the media increased inhibitor activity 3.04 \ m=+-\ 0.39 times compared with the control; however, A23187 (10 and 100 \g=m\mol l\m=-\1 ), in the presence of LH, decreased inhibitor activity by approximately 67%. The ionophore had disparate effects on progesterone production. Without LH, A23187 increased progesterone production by 2.96 \ m=+-\ 0.47 times at 10 \g=m\mol l\m=-\1and by 5.53 \ m=+-\ 0.65 times at 100 \g=m\mol l \ m=-\ 1 . However, in LH-stimulated cells, progesterone was inhibited by A23187 at 1 and 10 \g=m\mol l\m=-\1but was unchanged at 100 \g=m\mol l \m=-\1. In the angiotensin experiment, addition of AII (0\p=n-\10 000 nmol l\m=-\1 ) or saralasin (1 \g=m\mol l\m=-\1 ) did not affect inhibitor activity or progesterone concentrations compared with control values in the absence or presence of LH. For the angiotensin experiment in vivo, PMSG-primed rats were injected with hCG followed by saralasin (10 mmol l \ m=-\ 1 ) 1 or 3 h later and killed at 4, 8, or 12 h after hCG. Expression of the ovarian tissue inhibitor of metalloproteinase-1 (TIMP-1) increased by 1.7 times at 4 h, 3.3 times at 8 h, and 3.0 times at 12 h after hCG compared with values in ovaries collected at the time of hCG injection. Administration of saralasin at 1 or 3 h after hCG had no effect on expression of TIMP-1 or on serum concentrations of progesterone or oestradiol. In summary, A23187 decreased granulosa cell-derived inhibitor activity, whereas AII had no effect. We propose that calcium may play a role in modulating proteolysis associated with ovulation, while AII does not appear to regulate ovarian metalloproteinase inhibitor activity.
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