Inhibition of ovulation in rabbits by intrafollicular injection of indomethacin and prostaglandin F antiserum

Armstrong, David T.; Grinwich, Daniel L.; Moon, Young Soo; Zámečník, Jiří

doi:10.1016/0024-3205(74)90252-5

Cited by 119 publications

(21 citation statements)

References 24 publications

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“…There is little doubt that PGs can act at the level of the ovary [1], but investigations into the pos sible central action of PGs, at the level of the hypothalamus, have produced conflicting re sults [17]. The present experiments are con sistent with in vivo evidence which supports a central mediation of PGs in ovulation in the rat.…”

Section: Discussionsupporting

confidence: 62%

Prostaglandins and the Release of LHRH from Hypothalamic Synaptosomes

Linton¹,

Bennett²,

Whitehead³

1979

Neuroendocrinology

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The possible role of prostaglandins (PGs) in the hypothalamic control of ovulation has been investigated by studying the effects of indomethacin (ID) and PGs on the release of luteinizing hormone-releasing hormone (LHRH) from hypothalamic synaptosomes. Female rats were chronically pretreated with ID on diestrus 2 (D₂) and proestrus (P), or on diestrus 1 (D₁) and D₂. Basal LHRH release from hypothalamic synaptosomes prepared from rats pretreated on D₂/P was reduced to 48% after a 20-min incubation period, compared with sham-treated animals. ID pretreatment on D₁/D₂ caused a similar but less marked reduction in LHRH release (to 66% of controls at 20 min). Extraction of the LHRH remaining within the synaptosomal pellet showed that ID pretreatment also reduced the synaptosome content of LHRH. (15S)-15-methyl PGE₂ (15-E₂) (10^-4 and 10^–6 M) added to the incubating medium stimulated the release of LHRH by approximately 40%, but this effect was only observed in synaptosomes prepared from ID-treated rats. PGE₂ (10^–4 and 10^–6 M) had no significant effect in either sham-treated or ID-treated groups.

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Section: Discussionsupporting

confidence: 62%

Prostaglandins and the Release of LHRH from Hypothalamic Synaptosomes

Linton¹,

Bennett²,

Whitehead³

1979

Neuroendocrinology

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“…The ability of indomethacin (PG synthetase inhibitor) to block ovulation is documented for rats (Tsafriri et al, 1973), rabbits (O'Grady et al, 1972), sheep (Murdoch & Dunn, 1983) and cattle (De Silva & Reeves, 1985). Intrafollicular injection of PGF-2a antiserum blocked luteinizing hormone (LH)-induced ovulations in rabbits (Armstrong et al, 1974). However, in the present study active immunization against PGF-2a apparently did not inhibit follicular rupture in most of the cows.…”

Section: Discussioncontrasting

confidence: 60%

Effect of active immunization of pre-partum and post-partum cows against prostaglandin F-2 on lifespan and progesterone secretion of short-lived corpora lutea

Copelin¹,

Smith²,

Keisler³

et al. 1989

Reproduction

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“…Growing evidence suggests that PGs may be involved in the process of ovulation via local actions at the level of the ovary (41)(42)(43)(44). We recently found that the inhibition of Ang IIstimulated PG production by indomethacin led to the complete blockade of Ang II-induced ovulation (unpublished observations).…”

Section: Resultsmentioning

confidence: 99%

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

Yoshimura¹,

Koyama²,

Karube³

et al. 1994

J. Clin. Invest.

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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 ,uM 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 ,ug 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 Ang11 production in the rabbit ovary. Ovarian renin-angiotensin system may play an important role in the process of oocyte maturation after exposure to gonadotropin. (J.

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Inhibition of ovulation in rabbits by intrafollicular injection of indomethacin and prostaglandin F antiserum

Cited by 119 publications

References 24 publications

Prostaglandins and the Release of LHRH from Hypothalamic Synaptosomes

Prostaglandins and the Release of LHRH from Hypothalamic Synaptosomes

Effect of active immunization of pre-partum and post-partum cows against prostaglandin F-2 on lifespan and progesterone secretion of short-lived corpora lutea

Gonadotropin stimulates ovarian renin-angiotensin system in the rabbit.

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