Norihiro Koyama

Angiotensin II directly induces follicle rupture and oocyte maturation in the rabbit

To investigate the possible direct involvement of angiotensin II (Ang II) in ovulation and oocyte maturation, Ang II at 100 or 10 μg was administered at 2‐h intervals in the in‐vitro perfused rabbit ovaries. The addition of Ang II in the perfusate induced ovulation in vitro in the absence of gonadotropin, while ovulation did not occur in any contralateral control ovaries. However, the ovulatory efficiency in the Ang II‐treated ovaries was significantly lower than in hCG‐treated ovaries. Ang II significantly stimulated the meiotic maturation of ovulated ova and follicular oocytes. Concomitant addition of the specific receptor antagonist of Ang II, saralasin, 30 min before the onset of Ang II administration blocked Ang II‐induced ovulation in a complete manner. Although suralasin did not inhibit completely hCG‐induced ovulation and oocyte maturation, these results suggest that Ang II produced in the ovary may act locally in the process of ovulation.

Effects of growth hormone on follicle growth, oocyte maturation, and ovarian steroidogenesis

OBJECTIVES To assess the effects of GH on follicle growth, oocyte maturation, ovulation, and ovarian steroidogenesis. DESIGN In vitro perfused rabbit ovary. INTERVENTIONS The rabbit ovaries were perfused with medium alone, with GH at 1, 10, 100, or 200 ng/mL, or with 50 IU hCG for 12 hours. MAIN OUTCOME MEASURES The follicle diameter, the percent change in follicle diameter, the percentage of oocytes achieving germinal vesicle breakdown, and the production of P and E2 by the perfused rabbit ovaries. RESULTS The addition of GH to the perfusate increased the follicle diameter at 12 hours after perfusion in a dose-dependent manner. The percent change in follicle diameter in GH-treated ovaries did not differ significantly from that in hCG-treated ovaries at each time point of perfusion. However, ovulation did not occur in either the control ovaries or the experimental ovaries treated with GH. Exposure to GH at a concentration of > 10 ng/mL significantly stimulated the resumption of meiosis, as compared with the contralateral control ovaries. Although the concentration of P in the perfusate did not differ significantly between GH-treated and control ovaries, GH stimulated E2 production by the perfused rabbit ovaries in a dose-dependent manner. CONCLUSIONS Growth hormone acts on the rabbit ovary to stimulate follicle growth, oocyte maturation, and ovarian E2 production.

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit

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 hCG, compared with control ovaries perfused with medium alone. The level of intrafollicular Ang II after hCG exposure significantly exceeded the concentration of Ang II in an equivalent volume of plasma. The addition of 1 microM captopril to the perfusate significantly inhibited the secretion rate of Ang II stimulated by hCG; however, captopril affected neither the ovulatory efficiency nor prostaglandin production in ovaries treated with hCG. Captopril significantly inhibited the resumption of meiosis in the ovulated ova and follicular oocytes stimulated by hCG. The administration of 100 micrograms Ang II at 2-h intervals to the perfusate reversed the inhibitory effects of captopril on hCG-induced oocyte maturation. In conclusion, these data indicate that gonadotropin stimulates renin-like activity and Ang II production in the rabbit ovary. Ovarian renin-angiotensin system may play an important role in the process of oocyte maturation after exposure to gonadotropin.

Direct effect of gonadotropin-releasing hormone agonists on the rabbit ovarian follicle

OBJECTIVE To determine if gonadotropin-releasing hormone agonist (GnRH-a)-induced oocyte maturation and degeneration can be attributed to the direct actions on the follicle. DESIGN Mature rabbit follicle culture. INTERVENTIONS The mature follicles were cultured with human chorionic gonadotropin (hCG) (100 ng/mL), buserelin acetate (10(-9) to 10(-6) M), leuprolide acetate (10(-9) to 10(-6) M), or buserelin acetate (10(-7) M) with a GnRH antagonist (10(-8) to 10(-6) M) for 14 hours. MAIN OUTCOME MEASURES The percentage of oocytes achieving germinal vesicle breakdown, the oocyte degeneration rate, prostaglandins (PG) production by mature follicles, and the frequency of fertilization and embryonic development. RESULTS Gonadotropin-releasing hormone agonist induced the meiotic maturation of follicle-enclosed oocytes in a dose-dependent manner while concomitantly increasing oocyte degeneration. The simultaneous addition of GnRH antagonist inhibited significantly GnRH-a-induced oocyte maturation and PG production by the mature follicles. Furthermore, a GnRH antagonist reversed the oocyte degeneration rate that had been increased by GnRH-a. The rates of normal fertilization and early embryonic development were significantly reduced in the oocytes matured by GnRH-a as compared with those matured by hCG. CONCLUSIONS Gonadotropin-releasing hormone agonist acts directly on mature rabbit follicles to trigger the oocytes to undergo meiotic maturation, but oocytes matured in vitro by GnRH-a are not necessarily cytoplasmically mature.

Effects of Beta-1 Integrins in the Process of Implantation

The expression and function of beta 1 integrins on human decidual cells were investigated. Flow cytometric analysis revealed that the cultured decidual cells expressed a high level of the beta 1 subunit on the cell surface. Mouse blastocysts attached to and spread onto cultured human decidual cells. Attachment of the blastocysts was a necessary prerequisite for the further outgrowth of trophoblasts. The addition of a monoclonal antibody recognizing the beta 1 subunit to the cultured decidual cells did not affect the rates of hatching and attachment of blastocysts. The outgrowth of embryos on decidual cells was inhibited by the addition of the anti-beta 1-subunit antibody in a dose-dependent manner. Furthermore, exposure of decidual cells to the anti-beta 1-subunit antibody significantly inhibited the extent of outgrowth of trophoblasts, implying that blastocyst attachment and outgrowth is mediated by different mechanisms. These observations suggest that beta 1 integrins on decidual cells may be involved in the process of blastocyst development and differentiation after attachment.

Reversible intracranial changes in eclampsia demonstrated by MRI and MRA.

CT and MRI allow visualization of eclampsia changes in the brain. Once case with reversible changes is reported.

Possible Involvement of Lipoxygenase Products in Human Corpora lutea

The present study was undertaken to determine the ability of cultured luteal cells from human corpora lutea to secrete progesterone (P4) and prostaglandins (PGs), and to assess the effects of the products of the lipoxygenase pathway on luteal P4 production. Luteal cells responded to human chorionic gonadotropin (hCG) with a significant increase (2- to 7-fold) in P4 production. Arachidonic acid significantly stimulated PGE2 synthesis by luteal cells in a dose-dependent manner. Both basal PGE2 production and the responsiveness to arachidonic acid were maintained for 8 days. In contrast, both PGF2 alpha and 6-keto-PGF1 alpha production abruptly declined as the culture proceeded. However, the addition of hCG did not further stimulate the accumulation of the 3 PGs assayed. In the subsequent experiment, 5-hydroxyeicosatetraenoic acid (5-HETE) and the reaction products of soybean lipoxidase of arachidonic acid (AA-LIP) were utilized for evaluating the involvement of the lipoxygenase pathway in luteolysis. The addition of 5-HETE dose-dependently inhibited P4 production by the cultured luteal cells. Although treatment with either arachidonic acid or lipoxidase alone had no effect on P4 production, AA-LIP significantly reduced P4 production in the presence or absence of hCG. These results suggest that the products of the lipoxygenase as well as of the cyclo-oxygenase pathway may be important in regulating the life span and function of human corpora lutea.