INHIBITION OF PITUITARY PROLACTIN SECRETION BY HUMAN PLACENTAL LACTOGEN IN RATS

1976 ◽  
Vol 71 (1) ◽  
pp. 115-120 ◽  
Author(s):  
HIROSHI NAGASAWA ◽  
REIKO YANAI ◽  
KOREHITO YAMANOUCHI
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Placental Lactogen ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Corpora Lutea ◽  
Human Placental Lactogen ◽  
Vaginal Smears ◽  
Pituitary Prolactin

SUMMARY Intact female rats given twice daily injections of 1 mg human placental lactogen (HPL) showed continued dioestrous vaginal smears and their ovarian corpora lutea were found to be hypertrophied and functional. The serum prolactin level was significantly lower in these rats than in the controls at dioestrus as well as at pro-oestrus. Twice-daily injections of 0·5 or 2 mg HPL to ovariectomized rats decreased serum and pituitary levels of prolactin and increased hypothalamic activity of prolactin inhibiting hormone, although the effect was less at the lower dose. Human placental lactogen had no direct effect on pituitary prolactin secretion in vitro. These findings have demonstrated that HPL, like prolactin itself, inhibits prolactin secretion by acting indirectly on the pituitary through the hypothalamus.

Excess in vitro prolactin secretion by pituitary cells from ovariectomized old rats

1984 ◽  
Vol 247 (4) ◽  
pp. E483-E488
Author(s):  
M. Haji ◽  
G. S. Roth ◽  
M. R. Blackman
Keyword(s):  
In Vitro Release ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pituitary Cells ◽  
Lh Release ◽  
Old Rats

Various in vivo and in vitro pituitary lactotropic and gonadotropic functions were measured in mature (6-7 mo, normally cycling) and old (24 mo, constant diestrus) female Wistar rats. Serum prolactin (PRL) levels were higher (P less than 0.001), whereas luteinizing hormone (LH) values were similar (P greater than 0.05) in old versus mature rats both before and 3 days after ovariectomy. Serum PRL levels decreased significantly (P less than 0.005) postovariectomy only in the mature rats. The in vitro release of PRL and LH was measured for 4 days in primary adenohypophyseal cell cultures from the ovariectomized rats. Both basal and 17 beta-estradiol (E2)-stimulated PRL release (P less than 0.001) and production (P less than 0.005) were greater by cells from old rats. In contrast, both basal release and E2-stimulated LH release were greater (P less than 0.001) by cells from mature rats. Peak PRL release by cells from both old and mature rats occurred after exposure to E2 doses 1/100th of those required for peak LH release. These data support the hypothesis that intrinsic derangements in anterior pituitary function contribute to the reproductive decline in aging female rats and that different pituitary cell types exhibit discordant age changes in estrogenic sensitivity.

Indomethacin treatment prevents prolactin-induced luteolysis in the rat

1987 ◽  
Vol 112 (2) ◽  
pp. 317-322 ◽  
Author(s):  
J. E. Sánchez-Criado ◽  
K. Ochiai ◽  
I. Rothchild
Keyword(s):  
Corpus Luteum ◽  
Left Kidney ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Silicone Elastomer ◽  
Serum Prolactin ◽  
Corpora Lutea ◽  
Synthesis Inhibitor ◽  
Significant Difference ◽  
Indomethacin Treatment

ABSTRACT Adult female rats were hypophysectomized and their pituitary glands autotransplanted beneath the left kidney capsule on day 2 (day 1 was the day of ovulation). In such rats the pituitary secretes prolactin fairly constantly and the corpora lutea secrete progesterone for several months. To induce the luteolytic effect of prolactin the rats were first injected s.c. with 2-bromo-α-ergocryptine (CB-154) on cycle days 12, 13 and 14 (i.e. 10, 11 and 12 days after operation) to depress prolactin secretion, and then with CB-154 vehicle (70% ethanol) daily until cycle day 21, to allow prolactin secretion to resume. One ovary was removed from each rat on day 15 and the remaining one on day 22. The mean (± s.e.m.) weight of the corpora lutea on day 15 was 1·46±0·06 mg and 0·98±0·07 mg on day 22 (n = 17). In contrast, rats in which the CB-154 treatment was maintained to day 21 had corpora lutea which weighed 1·31 ±0·09 on day 15 and 1·47 ±0·08 mg on day 22 (n = 15). To investigate whether indomethacin, a prostaglandin synthesis inhibitor, affected the luteolytic action of prolactin, the experiment was repeated, but on day 15 (after the removal of one ovary) the groups in which CB-154 treatment was stopped, as well as the group in which CB-154 treatment was maintained, were each divided into two groups. In one, indomethacin-containing silicone elastomer wafers and, in the other, blank silicone elastomer wafers, were placed within the bursa of the remaining ovary. There were no differences in corpus luteum weight on day 15 among any of these groups and the two groups of the first experiment. There was no significant difference in corpus luteum weight between day 15 and day 22 in any of the six groups except for the two groups treated with the CB-154 vehicle and not with indomethacin. Thus, treatment with indomethacin prevented the fall in corpus luteum weight associated with the discontinuation of CB-154 treatment. Serum prolactin levels fell until day 15 in all rats and remained low in those in which the CB-154 treatment was maintained to day 21, but returned to control values in those treated with vehicle after day 14. Serum progesterone levels fell and remained low in all groups. Indomethacin treatment had no effect on the levels of either serum prolactin or progesterone. We conclude that some of the pharmacological effects of indomethacin are to prevent prolactin-induced luteolysis, and we suggest that prolactin induces rapid regression of the corpus luteum by stimulating intraluteal prostaglandin production or by being necessary for the effect of luteolytic prostaglandins. J. Endocr. (1987) 112, 317–322

REDUCTIVE PATHWAYS OF PROGESTERONE METABOLISM IN THE RAT OVARY

1972 ◽  
Vol 69 (1) ◽  
pp. 141-152 ◽  
Author(s):  
A. Zmigrod ◽  
H. R. Lindner ◽  
S. A. Lamprecht
Keyword(s):  
Hydroxysteroid Dehydrogenase ◽  
Prolactin Secretion ◽  
Ovariectomized Rats ◽  
Corpora Lutea ◽  
Microsomal Preparation ◽  
Progesterone Metabolism ◽  
Rat Ovary ◽  
Reducing Activity ◽  
Pituitary Prolactin

ABSTRACT Progesterone underwent extensive reductive metabolism when incubated with a microsomal preparation from rat ovaries in the presence of NADPH. The major products formed were 3β-hydroxy-5α-pregnan-20-one, 5α-pregnane-3,20-dione and 5α-pregnane-3β,20α-diol. Newly formed corpora lutea of pregnancy were almost devoid of any microsomal A-ring reducing activity (5α-reductase and a 3β-hydroxysteroid dehydrogenase) and of soluble 20α-hydroxysteroid dehydrogenase. The behaviour of the A-ring reducing enzymes paralleled that of 20α-ol dehydrogenase in that their activity (i) was high during the oestrous cycle; (ii) declined between the third and seventh day of pregnancy; and (iii) increased sharply in corpora lutea of pregnancy when ergocornine – a drug blocking pituitary prolactin secretion – was given to the rats, yet remained low when prolactin and ergocornine were administered concurrently. However, the A-ring reducing activity did not show the sharp pre-partum rise exhibited by 20α-ol dehydrogenase, thus deviating from a pattern compatible with a co-ordinate control of the three enzymes involved in the metabolic inactivation of progesterone. Contrary to a report in the literature, 5α-pregnane-3,20-dione (20 mg/rat/day) was found to be ineffective when tested for pregnancy or deciduoma supporting activity in ovariectomized rats. The microsomal reductases, if indeed operative in vivo, may restrict the availability of progesterone as an oestrogen precursor.

ONSET OF OESTROGEN-INDUCED PROLACTIN SECRETION AND DNA SYNTHESIS BY THE RAT PITUITARY GLAND

1977 ◽  
Vol 72 (1) ◽  
pp. 35-39 ◽  
Author(s):  
JOAN JACOBI ◽  
H. M. LLOYD ◽  
J. D. MEARES
Keyword(s):  
Dna Synthesis ◽  
Pituitary Gland ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Serum Prolactin ◽  
Rat Pituitary ◽  
The Times ◽  
Pituitary Prolactin

SUMMARY The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.

Human placental lactogen directly inhibits rat cartilage growth processes in vivo and in vitro

1993 ◽  
Vol 128 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Mimi H Chiang ◽  
Kevin M Kelley ◽  
Charles S Nicoll
Keyword(s):  
Cartilage Explants ◽  
Female Rats ◽  
Placental Lactogen ◽  
Human Placental Lactogen ◽  
Cartilage Growth ◽  
Growth Processes ◽  
Peripheral Tissues ◽  
Placental Hormone

We have recently reported that human placental lactogen inhibits the growth of young female rats without changing the serum levels of insulin like growth factor-I. Accordingly, experiments were conducted to determine whether human placental lactogen could directly inhibit cartilage growth processes in vivo and in vitro. Osmotic minipumps with attached polyethylene catheters were used to infuse the hormone for seven days into the left hindlimb of three-month-old female rats via the common iliac artery. The right hindlimb of each animal served as an internal control. Infusion of the placental lactogen at 10 μg/rat/day caused a slight (10%) but significant decrease in the width of the tibial epiphysial cartilage plate and a higher dose (100 μg/rat/day) caused a greater degree of inhibition (25%). However, the higher dose also inhibited the tibial cartilage plate of the contralateral (non-infused) limb. The possibility that human placental lactogen could directly inhibit cartilage anabolic activity in vitro was evaluated by measuring the incorporation of 35SO4 into costal cartilage explants from three to four-month-old female rats. The placental hormone inhibited the incorporation of 35SO4 in a dose-related manner at concentrations ranging from 1.0 to 100 μg/l. As a test of the specificity of this inhibition the effect of the hormone on the incorporation of 35SO4 into cartilage explants from Coho salmon was determined. The placental lactogen did not affect incorporation of the sulfate into the fish cartilage over a range of doses from 1.0 to 1000 μg/l. These results indicate that at least some of the inhibitory effects of human placental lactogen on the growth of rats is direct on peripheral tissues, such as cartilage. This effect may be mediated by the well-established anti-insulin action of the placental hormone.

Effect of acute immunoneutralization of endogenous leptin on prolactin and LH secretion during the afternoon of pro-oestrus or in steroid-treated ovariectomized female rats

Reproduction ◽  
2000 ◽  
pp. 39-45 ◽  
Author(s):  
LC Gonzalez ◽  
L Pinilla ◽  
M Tena-Sempere ◽  
C Dieguez ◽  
FF Casanueva ◽  
...  
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Blood Samples ◽  
Lh Release ◽  
Lh Secretion

Recent data indicate that leptin is involved in the control of reproductive function. Experiments were carried out to analyse the role of endogenous leptin in the regulation of LH and prolactin secretion during the afternoon of pro-oestrus and that induced by ovarian steroids in ovariectomized rats. In the first experiment, cyclic female rats were implanted with intra-auricular and intracerebroventricular (i.c.v.) cannulae and, at pro-oestrus, were injected (i.c.v.) with 10 microliters normal rabbit serum or leptin antiserum (at 13:00 and 14:00 h). Blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the second experiment, female rats in pro-oestrus were injected with normal rabbit serum or leptin antiserum at 16:00 and 18:00 h and blood samples were taken every 10 min between 18:00 and 20:00 h. In the third experiment, adult female rats that had been ovariectomized 2 weeks before were implanted with intra-auricular and i.c.v. cannulae and treated with oestradiol benzoate (30 micrograms s.c.) at 10:00 h and progesterone (2 mg s.c.) 48 h later. Normal rabbit serum (10 microliters) or leptin antiserum (10 microliters) were injected (i.c.v.) at 13:00 and 14:00 h, and blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the fourth experiment, hemipituitaries from ovariectomized steroid-treated female rats were incubated in the presence of leptin116-130 (an active fragment of the native molecule), GnRH or leptin + GnRH. Prolactin and LH secretion during the afternoon of pro-oestrus in females treated with leptin antiserum was similar to that observed in animals injected with normal rabbit serum. In ovariectomized female rats, the steroid-induced LH surge increased slightly after administration of leptin antiserum, whereas the prolactin surge remained unchanged. In vitro, leptin116-130 (10(-5) to 10(-8) mol l-1) inhibited LH secretion and modulated the effect of GnRH on LH release, depending on the concentration of GnRH: leptin116-130 (10(-6) mol l-1) reduced the effectiveness of 10(-7) mol GnRH l-1 and increased that of 10(-9) mol GnRH l-1. In conclusion, these experiments indicate that acute immunoneutralization of endogenous leptin does not interfere with spontaneous or steroid-induced LH and prolactin surges. In addition, the finding that leptin116-130 inhibited LH release and modulated the effectiveness of GnRH in vitro provides evidence of the direct modulatory role of leptin on LH secretion acting at the pituitary.

Size heterogeneity of prolactin secreted from and stored in the rat anterior pituitary gland in vitro

1984 ◽  
Vol 4 (2) ◽  
pp. 129-137 ◽  
Author(s):  
Andrew M. Bentley ◽  
Teresa K. Surowy ◽  
Michael Wallis
Keyword(s):  
Anterior Pituitary ◽  
Relative Proportion ◽  
Gel Filtration ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Pituitary Glands ◽  
Dimeric Form ◽  
Size Heterogeneity ◽  
Pituitary Prolactin

The size heterogeneity of rat pituitary prolactin was investigated using anterior pituitary glands from female rats incubated in vitro and gel filtration on Sephadex G-100. Monomeric prolactin was preferentially secreted compared with dimeric and ‘trimeric” material. When glands were incubated with dopamine, prolactin secretion was inhibited and the relative proportion of dimer in the gland (but not the medium) was decreased. Morphine sulphate reversed the effect of dopamine on prolactin secretion and on the proportion of prolactin in the gland that was in the dimeric form. The results suggest that monomeric prolactin is more readily secreted than dimer, and that dopamine decreases the production or stability of the dimer.

Effect of the progesterone antagonist mifepristone on the hypothalamo-hypophysial-ovarian axis in rats

1990 ◽  
Vol 124 (3) ◽  
pp. 425-432 ◽  
Author(s):  
P. van der Schoot ◽  
J. Th. J. Uilenbroek ◽  
E. J. Slappendel
Keyword(s):  
Combined Treatment ◽  
Prolactin Secretion ◽  
Additional Treatment ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Corpora Lutea ◽  
Exogenous Oestrogen ◽  
Steroid Sensitive ◽  
Pituitary Enlargement ◽  
Progesterone Antagonist

ABSTRACT Treatment of female rats for 3 weeks with the antigestagen 1 1β-(4-dimethylaminophenyl)-17β-hydroxy-17α-(prop-1 -ynyl)-estra-4,9-dien-3-one (mifepristone) results in pituitary and ovarian enlargement. The present study dealt with the possible mechanism(s) of these responses. Ovarian enlargement appeared to be dependent upon prolactin. In the absence of prolactin, during combined treatment with mifepristone and the dopamine agonist 2-Br-α-ergokryptine, ovarian growth was significantly suppressed. It was unclear why persistent hyperprolactinaemia, due to treatment with mifepristone, resulted in persistence of functionally active corpora lutea despite intermittent ovulation, while persistent hyperprolactinaemia due to ectopic pituitary grafts did not. Pituitary enlargement appeared to be dependent upon the persistence of ovarian oestrogen secretion during the treatment period. Ovariectomy or lactation fully inhibited this response. Pituitary enlargement and prolactin secretion in ovariectomized rats in response to exogenous oestrogen (injections of oestradiol benzoate) were significantly enhanced by additional treatment with mifepristone. It is concluded that mifepristone facilitates the effect of oestrogen on pituitary lactotrophs, thereby enhancing pituitary growth. Ovarian enlargement during treatment with mifepristone may be specific for rats due to the luteotrophic action of prolactin in these animals. Pituitary enlargement due to facilitation of oestrogen-induced pituitary growth may become a focus of attention when this or similar antigestagenic drugs are being used for prolonged periods in clinical trials, e.g. for limiting steroid-sensitive tumour growth. Journal of Endocrinology (1990) 124, 425–432

EVIDENCE OF ANTAGONISM BETWEEN PROLACTIN AND GONADOTROPHIN SECRETION: EFFECT OF METHALLIBURE ON PERPHENAZINE-INDUCED PROLACTIN SECRETION IN OVARIECTOMIZED RATS

1971 ◽  
Vol 51 (4) ◽  
pp. 719-725 ◽  
Author(s):  
M. BEN-DAVID ◽  
A. DANON ◽  
F. G. SULMAN
Keyword(s):  
Combined Treatment ◽  
Virgin Female ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pituitary Cells ◽  
Similar Treatment ◽  
Gonadotrophin Secretion ◽  
High Doses

SUMMARY Perphenazine has previously been shown to stimulate prolactin secretion in intact and to a lesser degree in ovariectomized virgin female rats. The question whether the oversecretion of gonadotrophins (follicle-stimulating hormone and luteinizing hormone) occurring in ovariectomized animals interferes with the ability of the pituitary cells to secrete prolactin was investigated in sham-operated and ovariectomized rats after separate and combined treatment with methallibure (ICI-33828, a non-steroidal gonadotrophin suppressor) and perphenazine which served as a prolactin releaser. Pituitary and serum prolactin were measured simultaneously by radioimmunoassay. Serum prolactin detected at the end of 5 days' treatment with perphenazine (5 mg/kg/day, s.c.) was found to be increased (81 ng/ml) compared with controls (29 ng/ml). Similar treatment given to ovariectomized animals increased serum prolactin levels from 13·7 ng/ml to only 27 ng/ml. Although high doses of methallibure alone (20 mg/kg/day, s.c.) given to ovariectomized rats for 17 days restored prolactin secretion to the levels occurring in intact non-treated animals, a dose of 10 mg was ineffective. However, when 10 mg methallibure were given to perphenazine-treated ovariectomized rats, serum prolactin rose again to 80·1 ng/ml. These results provide substantial evidence that, when the pituitary is secreting high amounts of gonadotrophin, its prolactin secretion is reduced and its ability to secrete prolactin after perphenazine challenge is limited. Once the gonadotrophic oversecretion is suppressed, more prolactin is secreted and the pituitary can again secrete high amounts of prolactin when challenged by perphenazine. The results show that in rats there exists an antagonism between gonadotrophin and prolactin secretion.

Role of serotoninergic neurones in the control of gonadotrophin and prolactin secretion in the rat

1982 ◽  
Vol 94 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Csilla Ruzsas ◽  
Patrizia Limonta ◽  
L. Martini
Keyword(s):  
Combined Treatment ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Prolactin Release ◽  
Lh Secretion ◽  
The Brain

The role of brain serotonin (5-hydroxytryptamine, 5-HT) in the control of LH, FSH and prolactin secretion was studied in two groups of experimental animals: intact adult male rats and ovariectomized adult female rats. 5-Hydroxytryptophan (5-HTP), a precursor of serotonin synthesis, and fluoxetine, a specific inhibitor of 5-HT uptake, were given either alone or together. 5-Hydroxytryptophan (50 mg/kg) was administered intraperitoneally and fluoxetine (20 μg/rat) was given into one of the lateral ventricles of the brain. Neither 5-HTP nor fluoxetine given alone affected LH secretion but combined treatment with the two drugs elicited a significant increase in serum LH levels in both intact male and ovariectomized female rats. Fluoxetine and 5-HTP, alone or together, did not modify FSH secretion in either kind of animal. In intact males and in ovariectomized females, 5-HTP induced a significant increase in prolactin release; fluoxetine alone was ineffective. In male animals treated with fluoxetine plus 5-HTP, serum prolactin levels increased but such an increase was lower than that found in the animals treated only with 5-HTP. In ovariectomized rats, the combined treatment induced an increase in serum prolactin levels similar to that found in animals treated with 5-HTP alone. These data suggested that brain serotonin exerts a stimulating effect on LH secretion in both intact male and ovariectomized rats, but that it does not play any role in the control of FSH release in either kind of animal and that central serotoninergic pathways participate in the stimulating control of prolactin release from the anterior pituitary gland. However, some of the data also suggested the possibility of the existence in the brain of serotoninergic systems inhibiting prolactin secretion.

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