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Results for “Luteolytic Effects”

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PubMed1983

Role of the nongravid part of the uterus in the luteolytic effects of estrogen in pregnant rats.

Effects of a low dose of estradiol on the luteal function were studied in intact pregnant rats. The pregnant rats received daily sc injections of 0.1 microgram estradiol or sesame oil from day 7 to 14 of pregnancy (day 1 = day of insemination). Serum progesterone levels on day 15 were significantly lower in the estrogen-treated group than in the oil-treated group. In order to study how estrogen induced luteolysis, the pregnant rats received each of the following treatments on day 7 of pregnancy: (1) The uterus except that containing a single conceptus was removed by hysterectomy (hysterectomy group); (2) All but a single conceptus were removed by aspiration, so that rats carried only a single conceptus with the whole part of the nongravid uterus (aspiration group). Each group of rats received also sc injections of 0.1 microgram estradiol or sesame oil from day 7 to 14 of pregnancy. Estradiol treatment caused a significant decline in serum progesterone levels in the aspiration group on day 15, but this was not the case in the hysterectomy group. There was no significant difference in serum LH levels among any of the groups on day 15 of pregnancy. These results indicated that estradiol induced luteolysis in the intact pregnant rats, which would, at least in part, be mediated through the uterus.

Animals↗
PubMed2001

Cyclic changes in the responsiveness of regressing corpora lutea to the luteolytic effects of prolactin in rats.

In cyclic rats, apoptosis of luteal cells during structural luteolysis occurs cyclically at the transition from pro-oestrus to oestrus in response to the preovulatory prolactin surge. This finding indicates that cyclic changes in apoptosis during luteolysis are dependent on prolactin surge cyclicity. In this study, the effects of prolactin on structural luteolysis were studied under different experimental conditions in relation to the phase of the oestrous cycle. In rats treated with prolactin at metoestrus and dioestrus, apoptosis did not occur in regressing corpora lutea, whereas in rats treated with prolactin on the morning of pro-oestrus, a 12.3-fold and 3.4-fold increase were observed in the number of apoptotic cells in regressing corpora lutea of the current and previous oestrous cycles, respectively. However, when the preovulatory prolactin surge and hence the subsequent apoptotic burst were blocked, prolactin treatment at the dioestrus phase induced a 13-fold increase in the number of apoptotic cells and significant changes in the volume of the corpus luteum (38% decrease) and the number of steroidogenic cells per corpus luteum (70% decrease). The results of this study indicate that the responsiveness of the regressing corpus luteum to the pro-apoptotic effects of prolactin are dependent on the phase of the oestrous cycle and on the presence or absence of an apoptotic burst in response to the preovulatory prolactin surge on the evening of pro-oestrus. Steroidogenic cells surviving to the apoptotic burst during the transition from pro-oestrus to oestrus became refractory to the lytic effect of prolactin. Furthermore, these cells also responded to the luteotrophic effects of prolactin, reaching full morphological luteinization, as indicated by the rescue of regressing cyclic corpora lutea during pregnancy.

Animals↗
PubMed1996

Luteolytic effect of LH: inhibition of 3 beta-hydroxysteroid dehydrogenase and stimulation of 20 alpha-hydroxysteroid dehydrogenase luteal activities in late pregnant rats.

The mechanisms associated with the onset of luteolysis in the pregnant rat are not well known. The effect of a specific rat LH antiserum (AS-rLH) and of ovine LH (oLH) on luteal steroidogenesis on day 19 of pregnancy was examined. Rat LH antiserum administered intrabursally at 1000-1100 h on day 19 of pregnancy prevented the physiological decrease in 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity, the increase in 20 alpha-hydroxysteroid dehydrogenase (20 alpha-HSD) activity and the fall in serum progesterone (P4) level observed at 1800 h on day 21 of pregnancy. To see if oLH has a direct effect on luteal steroidogenesis, the gonadotrophin was injected into the periovarian bursa. The intrabursa treatment with 1 microgram oLH on day 19 of pregnancy at 0800-0900 h did not modify corpus luteal function 36 h after treatment, but treatment with 4 micrograms oLH per ovary induced a significant progressive decrease in luteal 3 beta-HSD activity starting 12 h after treatment, while a significant increase in 20 alpha-HSD activity, concomitant with a decrease in serum P4 level, occurred 48 h after treatment. Luteal P4 content decreased with respect to control groups 36 and 48 h after intrabursal treatment with 4 micrograms oLH. The intrabursal administration of 8 micrograms oLH induced an increase in 20 alpha-HSD activity and a decrease in 3 beta-HSD activity 36 h after treatment. Administration of 4 micrograms oLH per ovary on day 8 of pregnancy induced a significant increase in serum P4 levels without modifying 3 beta-HSD activity. In rats treated with oLH on day 19 of pregnancy the decrease in 3 beta-HSD activity occurred 36 h before the significant increase in 20 alpha-HSD activity and serum P4 level. In conclusion, the luteal enzymatic activity changes and the significant decrease in the intraluteal P4 concentration induced by the intrabursal administration of oLH and the clear effect of AS-rLH preventing the physiological luteal changes preceding parturition provide good evidence of an intraovarian action of LH during the normal progression of luteolysis in late pregnant rats.

20-Hydroxysteroid Dehydrogenases↗