Evidence for a luteolytic function of prolactin in the intact cyclic rat using 2-Br-α-ergokryptine (CB 154)

E, Billeter; Flückiger, E.

doi:10.1007/bf02137315

Cited by 56 publications

(13 citation statements)

References 6 publications

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“…On the other hand, precocipus (<2 days) administration of PRL to hypophysectomized rats in which ovulation had been induced by pretreatment with FSH and LH maintained functional corpora lutea (26). It has also been shown that PRL exerts a luteolytic effect in intact cycling rats HORMONAL REGULATION OF RAT OVARY 3/J-HSD Endo • 1990 Vol 127 • No 6 (27,28). In intact rats, hypoprolactinemia resulting from the administration of ergocornine to cycling rats for 15 days resulted in significant enlargement of the ovaries due to the accumulation of many old corpora lutea (29).…”

Section: /3-hsd Expression and Activity In Interstitial Cellsmentioning

confidence: 93%

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

et al. 1990

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The enzyme 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase (3 beta-HSD) catalyzes an obligatory step in the conversion of pregnenolone and other 5-ene-3 beta-hydroxysteroids into progesterone as well as precursors of all androgens and estrogens in the ovary. Since 3 beta-HSD is likely to be an important target for regulation by pituitary hormones, we have studied the effect of chronic treatment with LH (hCG), FSH, and PRL on ovarian 3 beta-HSD expression and activity in hypophysectomized adult female rats. Human CG (hCG) [10 IU, twice a day (bid)], ovine FSH (0.5 microgram, bid), and ovine PRL (1 mg, bid) were administered, singly or in combination, for a period of 10 days starting 15 days after hypophysectomy. In hypophysectomized rats, PRL exerted a potent inhibitory effect on all the parameters studied. In fact, PRL caused a 81% decrease in ovarian 3 beta-HSD mRNA content accompanied by a similar decrease in 3 beta-HSD activity and protein levels. In addition, ovarian weight decreased by 40% whereas serum progesterone fell dramatically from 1.92 nmol/liter to undetectable levels after treatment with PRL. Whereas hCG alone had only slight stimulatory effects on 3 beta-HSD mRNA, protein content and activity levels, treatment with the gonadotropin partially or completely reversed the potent inhibitory effects of oPRL on all the parameters measured. FSH, on the other hand, had no significant effect on 3 beta-HSD expression and activity. In situ hybridization experiments using the 35S-labeled rat ovary 3 beta-HSD cDNA probe show that the inhibitory effect of PRL is exerted primarily on luteal cell 3 beta-HSD expression and activity. On the other hand, it can be seen that hCG stimulates 3 beta-HSD mRNA accumulation in interstitial cells. The present data show that hCG and PRL exert potent and opposite cell-specific effects on ovarian 3 beta-HSD expression, activity, and content in the rat ovary. Moreover, the present study could suggest that female infertility associated with hyperprolactinemia in women could well be related, at least in part, to the potent inhibitory effect of PRL on ovarian 3 beta-HSD expression and activity.

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Section: /3-hsd Expression and Activity In Interstitial Cellsmentioning

confidence: 93%

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

et al. 1990

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“…rats by exogenous PRL administration. Conversely, luteolytic changes can be inhibited by blocking the preovulatory PRL surge with the dopaminergic agonist CB154 [2,4,12].…”

Section: Introductionmentioning

confidence: 97%

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

Gaytán¹,

Bellido²,

Morales³

et al. 2001

Biology of Reproduction

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We studied the morphological and quantitative changes in cyclic corpora lutea (CCL) and in CL of pregnancy (CLP) during structural luteolysis. Elimination of CCL takes several cycles, and cell death occurs as successive apoptotic bursts, from 2100 h in proestrus to 1300 h in estrus. Each apoptotic burst determined a 60% decrease in the CL volume and an 80% decrease in the number of steroidogenic cells (SC). All these changes were inhibited by blocking the preovulatory prolactin (PRL) surge with bromocryptine (CB154). Neither apoptotic cells nor changes in the number of SC were found in regressing CLP from Day 21 of pregnancy to Day 2 postpartum, although there was a 50% decrease in the CLP volume and a 30% decrease in the mean cross-sectional area of SC. Treatment with CB154 on the day of parturition did not modify these regressive changes. On Day 5 postpartum, the volume of the CLP and the number of SC were equivalent in lactating rats (showing high PRL concentrations induced by pup suckling) and nonlactating noncycling rats (in which cyclicity and, therefore PRL surges, were blocked by treatment with LHRH antagonist). However, on Day 10 postpartum, the CLP volume and the number of SC were significantly decreased in lactating rats, and apoptotic cells were frequent. In postpartum cycling rats, the CLP did not show apoptotic cells on the day of the second postpartum estrus (on Day 5 postpartum), whereas on the day of the third postpartum estrus (on Day 9 postpartum), apoptotic cells were abundant. These results indicate that PRL does not induce apoptosis in the CLP before Day 5 postpartum and strongly suggest that the proapoptotic effect of PRL is dependent on the degree of differentiation of luteal cells.

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“…The search for a compound with specific antigalactic action and free of uterotonic and vascular effects led to the selection of Bromocriptin® (Sandoz CB-154). This compound was found to inhibit lactation and other prolactin-dependent mechanisms in the experimental animal, and prolactin secretion has been successfully suppressed in all vertebrates tested so far, including man (3)(4)(5)(6)(7). The inhibitory action of CB-154 is not dependent on an intact hypothalamo-pituitary connection since the drug reduces elevated serum prolactin levels in rats with pituitaries transplanted beneath the kidney capsule (Marko and Niederer, unpublished data) and it decreases the secretion from pituitaries implanted into mammary glands of mice (8).…”

mentioning

confidence: 96%

Clinical and Hormonal Response To Bromocriptin (CB-154) in the Galactorrhea Syndromes

Pozo

Varga

Wyss

et al. 1974

The Journal of Clinical Endocrinology & Metabolism

187

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Nine female patients with galactorrhea were selected for treatment with Bromocriptin® (CB-154), a specific inhibitor of prolactin secretion. Elevated plasma prolactin (hPRL) was found in 7 of these cases, whereas 2 exhibited values within normal limits. LHRH (100 fig) stimulation elicited plasma LH/FSH increases in 6 of the women who were amenorrheic prior to therapy, indicating a suprasellar cause for the patients' failure to cycle. After TRH (250 fig) stimulation, 5 women out of 6 exhibited a blunted hPRL response and 4 of them failed to show any elevations after administration of chlorpromazine. It was only in one patient who exhibited basal hPRL within the normal range, that an average response to TRH was elicited. The possible mechanisms explaining the low levels of pituitary stimulation obtained are discussed.Treatment with CB-154 (3-5 mg/day) induced a fall in serum hPRL accompanied by cessation of milk secretion in 8 patients. Menses were restored in 7 amenorrheic women and corpora lutea formation was confirmed by elevated plasma progesterone levels in 6 of them. One patient exhibiting normal serum hPRL and amenorrhea following the discontinuation of an oral contraceptive failed to resume menses under CB-154 therapy despite a fall in hPRL, suggesting that the mechanisms involved were not prolactin-dependent.Hyperprolactinemia and galactorrhea tended to recur when therapy was withheld, indicating to a certain extent persistent autonomy of the mechanisms involved. Since CB-154 has been found to inhibit not only prolactin secretion but also hormone synthesis, it remains to be seen whether long-term therapy with this agent may induce permanent remissions in patients with galactorrheaamenorrhea. (/ Clin Endocrinol Metab 39: 18, 1974)

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Evidence for a luteolytic function of prolactin in the intact cyclic rat using 2-Br-α-ergokryptine (CB 154)

Cited by 56 publications

References 6 publications

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

Clinical and Hormonal Response To Bromocriptin (CB-154) in the Galactorrhea Syndromes

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Evidence for a luteolytic function of prolactin in the intact cyclic rat using 2-Br-α-ergokryptine (CB 154)

Cited by 56 publications

References 6 publications

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ5-Δ4Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

Luteolytic Effect of Prolactin Is Dependent on the Degree of Differentiation of Luteal Cells in the Rat1

Clinical and Hormonal Response To Bromocriptin (CB-154) in the Galactorrhea Syndromes

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Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*

Regulation of 3β-Hydroxysteroid Dehydrogenase/Δ⁵-Δ⁴Isomerase Expression and Activity in the Hypophysectomized Rat Ovary: Interactions between the Stimulatory Effect of Human Chorionic Gonadotropin and the Luteolytic Effect of Prolactin*