Involvement of the adrenergic system on the release of prolactin and lactogenesis at the end of pregnancy in the rat

1991 ◽  
Vol 129 (3) ◽  
pp. 343-350 ◽  
Author(s):  
G. A. Jahn ◽  
R. P. Deis
Keyword(s):  
Mammary Gland ◽  
Placental Lactogen ◽  
Serum Prolactin ◽  
Adrenergic System ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Ru 486 ◽  
Prostaglandin F ◽  
Adrenergic Antagonists ◽  
Intact Rats

ABSTRACT The part played by the adrenergic system on the release of prolactin and lactogenesis induced by prostaglandin F2α and the antiprogesterone RU 486 was studied in pregnant rats. Two doses of prostaglandin F2α (150 μg) administered at 08.00 and 12.00 h on day 19 of pregnancy induced, at 12.00 h on day 20 (24 h after administration), a significant increase in the serum concentration of prolactin, with a significant decrease in serum progesterone levels. These hormonal changes significantly augmented casein and lactose levels in the mammary gland. Treatment with RU 486 (2 mg/kg) at 08.00 h on day 19 augmented casein and lactose concentrations in the mammary gland at 12.00 h on day 20 without modifying serum concentrations of prolactin and progesterone. The adrenergic antagonists, propranolol (3 mg/kg), metoprolol (10 mg/kg), ICI 118 551 (200 μg/kg), idazoxan (100 μg/kg) and prazosin (10 mg/kg), were administered s.c. at 12.00 and 20.00 h on day 19 and 08.00 h on day 20 of pregnancy to intact rats or to rats previously treated with RU 486 or prostaglandin F2α. These adrenergic antagonists did not modify serum prolactin or progesterone levels in intact or RU 486-treated rats, but serum prolactin levels in the prostaglandin F2α-treated group were significantly reduced by treatment with propranolol, metoprolol or prazosin. In addition, propranolol and ICI 118 551 also decreased the casein and lactose concentrations in the mammary glands of RU 486- and prostaglandin F2α-treated rats, while the other compounds had no effect. We also studied the effect of adrenergic antagonists on the release of prolactin and lactogenesis induced by the physiological decrease in progesterone at the end of pregnancy. On day 21 of pregnancy at 18.00 h, serum progesterone levels in intact rats were lower than 40 nmol/l, while serum prolactin and casein and lactose concentrations in the mammary gland were higher compared with values measured at 12.00 h on day 20. Treatments with propranolol, metoprolol or prazosin administered at 20.00 h on day 20 and 08.00 and 14.00 h on day 21 of pregnancy were capable of significantly reducing serum prolactin concentrations while only propranolol decreased mammary casein and lactose. The effect of propranolol was not mediated through a reduction in serum placental lactogen measured by Nb2 lymphoma cell bioassay. These results show that the adrenergic system participates, through α1 and β1 receptors, in the regulation of prolactin release induced by the decrease in progesterone in pregnant rats. They also show that β2-adrenergic receptors play a role in the induction of casein and lactose synthesis in the mammary gland. Journal of Endocrinology (1991) 129, 343–350

A modulatory role of endogenous opioids on prolactin secretion at the end of pregnancy in the rat

1994 ◽  
Vol 140 (1) ◽  
pp. 97-102 ◽  
Author(s):  
M Soaje ◽  
R P Deis
Keyword(s):  
Time Course ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Serum Prolactin ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Ru 486 ◽  
Prolactin Suppression

Abstract It is well known that the fall in serum progesterone concentrations during late pregnancy induces prolactin secretion in rats. On day 19 of pregnancy, administration of 10 mg of the antiprogesterone RU-486/kg induced a small but significant increase in serum prolactin. A lower dose (2 mg/kg) was not effective. Administration of naloxone (2 mg/kg) to pregnant rats on day 19 of pregnancy did not modify circulating prolactin but, after RU-486 treatment, a notable increase in serum prolactin was obtained 30 min after naloxone was given. The lack of effect of naloxone-methobromide in pregnant rats pretreated with RU-486 may indicate that the opioid-induced prolactin suppression acts centrally, most probably at the hypothalamic level. During day 21 of pregnancy, the time-course of prolactin secretion, measured at 0900, 1400, 1900 and 2200 h, was inversely correlated with circulating progesterone levels. At 0900 h, serum prolactin was very low with high serum progesterone concentrations but a significant increase in serum prolactin occurred at 2200 h; this was coincident with a significant decrease in the steroid. The stimulatory effect of naloxone on prolactin secretion was clearly dependent on the circulating progesterone level. Thus, at 1900 h of day 21, naloxone induced a significant increase in serum prolactin but, at 2200 h, the opioid antagonist dramatically enhanced the circulating level of prolactin. The serum prolactin increase induced by naloxone at 1900 h was prevented by the s.c. administration of 5 mg progesterone given 7 h earlier. Similarly, the large increase in serum prolactin levels at 1800 h on day 19 of pregnancy, after administration of RU-486 plus naloxone, was completely abolished by treatment with CB154. The lack of effect of RU-486 and naloxone on serum prolactin levels in virgin rats on the day of pro-oestrus demonstrates that the effect of naloxone on prolactin in pregnant rat is peculiar to the end of pregnancy. In conclusion, the attenuation of the central inhibitory action of progesterone facilitates the release of prolactin which is dramatically enhanced by naloxone treatment. These results provide an important new insight into the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy. Journal of Endocrinology (1994) 140, 97–102

Effects of chronic thyroid hormone administration on pregnancy, lactogenesis and lactation in the rat

1992 ◽  
Vol 127 (6) ◽  
pp. 547-554 ◽  
Author(s):  
Roberto R Rosato ◽  
Maria S Gimenez ◽  
Graciela A Jahn
Keyword(s):  
Mammary Gland ◽  
Maternal Behavior ◽  
Elevated Serum ◽  
Fatty Acid Synthetase ◽  
Milk Ejection ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Severe Reduction ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Gland Content

We studied the effects of daily administration of 1 mg/kg thyroxine (T4) starting 10–15 days before mating, on parturition, maternal behavior and lactation in rats. Treated rats had elevated serum titers of T3 and T4, a greater number of fetuses and parturition was advanced approximately 12 h and lasted longer than in controls. None of the treated rats were able to lactate because of defects in maternal behavior and milk ejection; the litters died usually within 48 h postpartum. In rats sacrificed at 10.00 on day 21 of pregnancy, mammary gland content of total protein, phospholipids, casein and lactose were significantly increased, but total lipid was markedly reduced. Lipogenesis was also significantly increased, as well as the activity of the lipogenic enzymes glucose-6-phosphate dehydrogenase, fatty acid synthetase and isocytrate dehydrogenase. These results are indicative of normal albeit premature lactogenesis. The T4-treated rats also had advances in the prepartum fall in serum progesterone and the increase in prolactin as well as in the increase in mammary casein and lactose concentrations of approximately 12 h with respect to control pregnant rats. These results show that chronic T4 treatment induces an advance of approximately 12 h in luteolysis, which in turn advances lactogenesis and parturition in rats. Although the mammary gland was able to produce milk, lactation failed due to abnormal maternal behavior and milk ejection, the causes of which are still unknown. Other effects of hyperthyroidism were also present, such as a severe reduction in lipid content of the gland. The observed increases in lipogenesis and lipogenic enzyme activities could be due to a combination of the effects of hyperthyroidism per se as well as to the increase in lipogenesis that occurs during lactogenesis.

scholarly journals γ-glutamyltransferase activity in mammary gland of pregnant rats and its regulation by ovarian hormones, prolactin and placental lactogen

1984 ◽  
Vol 223 (1) ◽  
pp. 275-277 ◽  
Author(s):  
L E Bussmann ◽  
R P Deis
Keyword(s):  
Enzyme Activity ◽  
Mammary Gland ◽  
Ovarian Hormones ◽  
Placental Lactogen ◽  
Pregnant Rats ◽  
Gamma Glutamyltransferase

Ovariectomy and ovariectomy plus hysterectomy on day 18 of pregnancy increased gamma-glutamyltransferase activity in the mammary gland. The withdrawal of progesterone and the subsequent release of prolactin are responsible for the rise in enzyme activity. Rat placental lactogen in the absence of prolactin and progesterone is able to induce gamma-glutamyltransferase activity.

THE SEQUENCE OF HORMONAL CHANGES DURING PROSTAGLANDIN INDUCED LUTEOLYSIS OF THE SUPERLUTEINIZED RAT OVARY

1978 ◽  
Vol 87 (3) ◽  
pp. 617-624 ◽  
Author(s):  
P. A. Torjesen ◽  
R. Dahlin ◽  
E. Haug ◽  
A. Aakvaag
Keyword(s):  
Binding Sites ◽  
Limit Of Detection ◽  
Serum Levels ◽  
Female Rats ◽  
Serum Prolactin ◽  
Hormonal Changes ◽  
Subsequent Increase ◽  
Serum Progesterone ◽  
Serum Lh ◽  
Prostaglandin F

ABSTRACT Immature female rats were pre-treated with pregnant mare's serum gonadotrophin (PMSG) and human chorionic gonadotrophin (HCG) to achieve superluteinization. Eight days after the HCG administration luteolysis was induced by sc injection of 5 μg of the prostaglandin F2α (PGF2α) analogue cloprostenol (Estrumate®). The serum levels of progesterone, 20α-dihydroprogesterone (20α-DHP), prolactin (PRL) and luteinizing hormone (LH) as well as the number of ovarian LH binding sites were measured during the first 23 h after cloprostenol injection. The serum levels of progesterone decreased from 500 to 200 ng/ml within 25 min after cloprostenol administration. A further decrease to 20 ng/ml occurred during the next 4 h, and serum progesterone remained low for the rest of the period. An increase in serum prolactin (PRL) to values between 28 and 44 ng/ml was observed after 3 h and the values remained elevated for the next 7 h. Although the serum levels of progesterone declined immediately, the serum 20α-dihydroprogesterone (20α-DHP) levels remained at 60 to 140 ng/ml for the first 5 h and then gradually increased to values corresponding to the initial progesterone levels 14 to 23 h after treatment. The number of ovarian LH binding sites was between 1.2 and 1.4 × 10−12 mol/mg protein during the first 9 h after prostaglandin (PG) injection, and then decrreased to 0.8 and 0.5 × 10−12 mol/mg protein at 14 and 23 h, respectively. The serum LH levels remained below the limit of detection for the assay (10 ng/ml) throughout the observation period. PGF2α injection induced the same basic changes in the serum levels of progesterone and 20α-DHP as cloprostenol treatment. Thus, the first effect of PG treatment measured was an immediate decline in the serum levels of progesterone, and this decline probably initiated the subsequent increase in pituitay PRL and ovarian 20α-DHP secretion. Therefore, the decrease in the number of ovarian LH binding sites appeared to be a consequence rather than a mediator of luteolytic effects of the prostaglandins.

Opioidergic regulation of prolactin secretion during pregnancy: role of ovarian hormones

1997 ◽  
Vol 155 (1) ◽  
pp. 99-106 ◽  
Author(s):  
M Soaje ◽  
RP Deis
Keyword(s):  
Ovarian Hormones ◽  
Prolactin Secretion ◽  
High Serum ◽  
Opioid System ◽  
Serum Prolactin ◽  
Stimulatory Action ◽  
Serum Progesterone ◽  
Naloxone Administration ◽  
Ru 486 ◽  
Naloxone Treatment

We have recently demonstrated the existence of a neuromodulatory regulation of prolactin secretion by the opioid system showing a paradoxical opioid-induced prolactin suppression at the end of pregnancy. The aim of this study was to determine a possible interaction between the opioid system and ovarian hormones on the release of prolactin during pregnancy. Serum prolactin levels measured at 1800 h were significantly higher on days 3 and 6 of pregnancy when compared with the other days of gestation. These increases in serum prolactin were reduced significantly by naloxone (2 mg/kg) administered at 1730 h and by RU-486 (10 mg/kg) administered at 0800 h. The response induced by RU-486 was potentiated by naloxone only on day 3. On days 7, 13 and 16, prolactin secretion was not modified by RU-486 and/or naloxone treatment. In RU-486 pretreated rats, naloxone administration increased serum prolactin levels only on day 16 of pregnancy. Interestingly, progesterone treatment (0.5 mg/rat) on days 13, 14 and 15 of pregnancy prevented the high increase in serum prolactin induced by RU-486 and naloxone on day 16 of pregnancy. The progressive increase and decrease of serum progesterone concentration during pregnancy was not modified by naloxone treatment. The participation of oestrogen in the regulation of prolactin secretion by the opioid system on days 3, 16 and 19 was examined by treating these groups of rats with oestradiol benzoate or tamoxifen citrate. Oestradiol (2 micrograms/rat) significantly increased serum prolactin levels on day 3 and naloxone administration did not modify this increase. No effect was observed after oestradiol (5 micrograms/rat) and naloxone treatment on days 16 and 19 of pregnancy. Oral administration of tamoxifen (500 micrograms/kg) the previous day did not modify the serum prolactin concentration measured at 1800 h in oil-treated rats on days 3, 16 and 19 of pregnancy. The antioestrogen completely abolished the naloxone-induced prolactin secretion on day 16 in rats pretreated with RU-486 but no effect was observed on day 19. When tamoxifen was administered on days 14 and 15 of pregnancy, the high serum prolactin levels on day 19 induced by treatment with RU-486 and naloxone were significantly reduced. In conclusion, these results provide an important new insight into the existence of a dual neuromodulatory regulation of prolactin secretion by the opioid system during pregnancy. After a stimulatory action during the first days, there is a change to an inhibitory control at the end of pregnancy, starting around day 16. Moreover, the activation of the inhibitory modulation of the opioid system on prolactin secretion on days 16 and 19 of pregnancy seems to be mediated by changes in the oestrogen and progesterone action.

Fluprostenol-induced softening of the cervix of the pregnant rat

1983 ◽  
Vol 97 (2) ◽  
pp. 283-290 ◽  
Author(s):  
L. M. Williams ◽  
M. Hollingsworth ◽  
M. Dukes ◽  
I. D. Morris
Keyword(s):  
Binding Capacity ◽  
Direct Action ◽  
Prostaglandin E ◽  
Uterine Contractility ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Uterine Contractions ◽  
Prostaglandin F

Fluprostenol, an analogue of prostaglandin F2α, administered s.c. to rats on day 18 of pregnancy increased cervical creep, or softness, by the following day. Doses of fluprostenol 100-fold larger were necessary to increase uterine contractions. Fluprostenol produced falls in serum progesterone concentrations, increases in 20α-dihydroprogesterone concentrations, no changes in oestradiol or relaxin concentrations and a reduction in the ovarian human chorionic gonadotrophin binding capacity in vitro. Fluprostenol was less potent in inducing cervical softness when administered per vaginam, and a dose which produced softening in pregnant rats was ineffective in ovariectomized steroid-maintained pregnant or pro-oestrous rats. The findings suggest that cervical softening by fluprostenol does not result from a simple direct action on the cervix or by increasing uterine contractions, but rather by an indirect hormonal action mediated by the ovaries. The results with the lowest dose of fluprostenol indicate that cervical softening could be produced without a sustained fall in serum progesterone concentrations. Fluprostenol is much more potent at increasing cervical softness in the pregnant rat than prostaglandin F2α or prostaglandin E2. With fluprostenol the ratio of dose to induce uterine contractility relative to that to produce cervical softness was greater than with these natural prostaglandins, indicating the greater selectivity of fluprostenol in the pregnant rat.

INHIBITORY EFFECT OF PROGESTERONE ON THE LACTOGENIC AND ABORTIVE ACTION OF PROSTAGLANDIN F2α

1975 ◽  
Vol 66 (1) ◽  
pp. 21-29 ◽  
Author(s):  
NELIA T. VERMOUTH ◽  
R. P. DEIS
Keyword(s):  
Single Dose ◽  
Plasma Concentration ◽  
Prostaglandin F2α ◽  
Inhibitory Effect ◽  
Induced Abortion ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Pregnant Rats ◽  
Unilateral Ovariectomy ◽  
Prostaglandin F

SUMMARY The effect of ovariectomy, progesterone and prolactin treatment on the action of prostaglandin F2α (PGF2α) was determined in pregnant rats. PGF2α (150 μg × 2) injected i.p. on day 19 or 18 of pregnancy induced lactogenesis about 25 h later and abortion on days 20 and 21 of pregnancy. Treatment with PGF2α (100 μg × 2 or 50 μg × 2) on day 19 induced lactogenesis around 22 or 38 h later, respectively, and abortion on day 21. PGF2α treatment on day 17 was less effective. Unilateral ovariectomy on day 17 of pregnancy induced lactogenesis 32 h later but not abortion. PGF2α (150 μg × 2) given on the day of surgery advanced lactogenesis 12 h and rats aborted on day 19. Bilateral ovariectomy on day 17 induced abortion between days 20 to 21, but if a single dose of PGF2α (300 μg) was injected on day 18, all the ovariectomized rats aborted on day 19. Progesterone (10 mg) injected into rats treated with PGF2α (150 μg × 2) on day 18, prevented abortion and delayed lactogenesis. Prolactin (1 mg × 4) treatment delayed only abortion. Serum prolactin levels were significantly higher 12 h after the last dose of PGF2α (150 μg × 2) in rats treated on days 17, 18 or 19 of pregnancy. Pretreatment with progesterone prevented the rise in prolactin concentration. These results suggest that the lactogenic and abortive action of PGF2α may be dependent on the uterine and plasma concentration of progesterone.

Potentiation by prolactin of the luteotrophic effect of oestradiol in the pregnant rat

1982 ◽  
Vol 101 (2) ◽  
pp. 287-292 ◽  
Author(s):  
Richard G. Rodway ◽  
David R. Garris
Keyword(s):  
Sampling Period ◽  
Daily Treatment ◽  
Serum Prolactin ◽  
Renal Capsule ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Luteal Function ◽  
Progesterone Secretion

Abstract. The luteotrophic effects of elevated prolactin levels with or without concomitant oestradiol treatment were investigated in the pregnant rat after hysterectomy or hysterectomy plus hypophysectomy. On day 2 of pregnancy, rats were given a single pituitary transplant beneath the renal capsule and were subsequently hysterectomised on day 12. This treatment delayed the next ovulation (as judged by vaginal di-oestrus length) compared to sham-transplanted controls, but did not prevent the fall in serum progesterone concentrations (i.e. luteolysis) resulting from hysterectomy. The administration of 1 or 2 pituitary homo-transplants on day 12 at the time of hysterectomy again prolonged the di-oestrus length but did not prevent subsequent luteolysis. However, daily treatment with 100 μg of oestradiol given to rats which received 2 pituitary transplants on day 2 and which were then hysterectomised on day 12, did result in a maintenance of serum progesterone levels compared to those of oil-treated controls. In a separate study, pregnant rats were hysterectomised and hypophysectomised on day 12. Administration of either 1 or 2 pituitary transplants failed to maintain luteal function. However, concomitant daily treatment with 100 μg of oestradiol from day 12 onward prevented luteolysis and re-instated the day 12–16 rise in serum progesterone common to the intact pregnant rat. Progesterone levels then declined slowly until the end of the sampling period (day 23). Serum prolactin concentrations rose steadily for the first 10 days after insertion of pituitary transplants on day 12 of pregnancy. These data indicate that prolactin and oestradiol can act synergistically to stimulate progesterone secretion from the rat corpus luteum but only in the absence of the in situ pituitary; the effect is not seen unless hypophysectomy has been performed.

scholarly journals Growth-hormone-prolactin interactions in the regulation of mammary and adipose-tissue acetyl-CoA carboxylase activity and gene expression in lactating rats

1992 ◽  
Vol 285 (2) ◽  
pp. 469-475 ◽  
Author(s):  
M C Barber ◽  
M T Travers ◽  
E Finley ◽  
D J Flint ◽  
R G Vernon
Keyword(s):  
Adipose Tissue ◽  
Mammary Gland ◽  
Serum Prolactin ◽  
Acetyl Coa Carboxylase ◽  
Acetyl Coa ◽  
Carboxylase Activity ◽  
Total Enzyme Activity ◽  
Mrna Concentration ◽  
Total Enzyme ◽  
Activation Status

The factors and mechanisms responsible for the reciprocal changes in lipogenesis in rat mammary gland and adipose tissue during the lactation cycle have been investigated. Lactation decreased the activation status and mRNA concentration of acetyl-CoA carboxylase in adipose tissue. Litter removal decreased the mRNA concentration of acetyl-CoA carboxylase in the mammary gland and increased the enzyme's mRNA concentration and activation status in adipose tissue. Lowering serum prolactin concentration in lactating rats decreased the amount of mammary acetyl-CoA carboxylase mRNA and increased that of adipose tissue, and increased the activation status of the enzyme in adipose tissue. Decreasing serum growth hormone (GH) alone had little effect on acetyl-CoA carboxylase in lactating rats, although it did lower pup growth rate and serum concentration of insulin-like growth factor-I. Lowering serum GH concentration exacerbated the effects of decreasing serum prolactin on mammary-gland (but not adipose-tissue) acetyl-CoA carboxylase mRNA and further increased the rise in activation status of the adipose-tissue enzyme induced by decreasing serum prolactin. Changes in acetyl-CoA carboxylase mRNA in both mammary and adipose tissue were paralleled by changes in total enzyme activity except after litter removal, when there was a disproportionately large decrease in total enzyme activity of the mammary gland. Thus prolactin has a major and GH a minor role in the regulation of acetyl-CoA carboxylase activity during lactation. Changes in mammary activity in response to prolactin and GH are primarily due to alterations in gene transcription, whereas adaptation in adipose tissue involves both changes in gene transcription and activation status.

scholarly journals Serum Progesterone in Pregnant Rats with Ectopic or in situ Corpora Lutea: Correlation Between Amount of Luteal Tissue and Progesterone Concentration1, 2

1975 ◽  
Vol 13 (5) ◽  
pp. 541-545 ◽  
Author(s):  
David J. Elbaum ◽  
Edward M. Bender ◽  
Judith M. Brown ◽  
P. Landis Keyes
Keyword(s):  
Corpora Lutea ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Luteal Tissue
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