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

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.

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.

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

Regulation of the photoperiod-induced cycle in the peripheral blood concentrations of β-endorphin and prolactin in the ram: role of dopamine and endogenous opioids

1990 ◽  
Vol 127 (3) ◽  
pp. 461-469 ◽  
Author(s):  
E. Ssewannyana ◽  
G. A. Lincoln
Keyword(s):  
Plasma Concentrations ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Fold Change ◽  
Opioid Antagonist ◽  
Light Cycle ◽  
Blood Concentrations ◽  
The Mean ◽  
Short Days

ABSTRACT In a group of adult Soay rams housed indoors under an artificial light cycle of alternating 16-week periods of long and short days, there was a conspicuous longterm cycle in the peripheral plasma concentrations of β-endorphin and prolactin. The levels of β-endorphin were highest under short days and lowest under long days (15-fold change), and inversely related to the changes in the plasma levels of prolactin (120-fold change). The role of dopamine in the control of β-endorphin and prolactin was investigated in a series of experiments, conducted under both long and short days, in which rams were treated with dopamine receptor agonists (dopamine and bromocriptine) and antagonists (pimozide and sulpiride). Naloxone (opioid antagonist) was also administered to assess the additional involvement of endogenous opioids. Dopamine injected i.v. (6·6 mg/kg every 10 min) did not significantly affect the mean plasma concentrations of β-endorphin and prolactin under either long or short days. Pimozide (0·08 mg/kg i.m. every 2 h) caused a large increase in the mean plasma concentrations of β-endorphin and prolactin under long days but not short days. Naloxone (1·6 mg/kg, i.v.), administered alone or in combination with dopamine or pimozide, had no effect on the mean plasma concentrations of β-endorphin and prolactin, except under short days when, combined with pimozide, it induced an increase in the plasma concentrations of the two polypeptides. Bromocriptine (0·06 mg/kg, s.c.) caused a significant decrease in the plasma concentrations of both β-endorphin and prolactin; this effect was most marked at the times of increased secretion (under short days for β-endorphin and under long days for prolactin). Sulpiride (0·59 mg/kg, s.c.) produced the converse effect and caused an increase in the plasma concentrations of β-endorphin and prolactin with the amplitude and duration of the effect varying with the stage of the photoperiod-induced cycle. From these results in the Soay ram, we conclude that dopamine inhibits β-endorphin and prolactin secretion by way of D2 receptors under both long and short days. Endogenous opioids interact with dopamine, augmenting this inhibition under short days. Differences in the acute responses in the secretion of β-endorphin and prolactin, and the inverse relationship between β-endorphin and prolactin during the cycle, indicate that different regulatory systems involving dopamine influence the two pituitary polypeptides. Journal of Endocrinology (1990) 127, 461–469

Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men

1994 ◽  
Vol 131 (1) ◽  
pp. 50-55 ◽  
Author(s):  
V Coiro ◽  
R Volpi ◽  
ML Maffei ◽  
A Caiazza ◽  
G Caffarri ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Physical Exercise ◽  
Sodium Valproate ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Aminobutyric Acid ◽  
Opioid Antagonist ◽  
Gamma Aminobutyric Acid ◽  
Normal Men ◽  
Plasma Gh

Coiro V, Volpi R, Maffei ML, Caiazza A, Caffarri G, Capretti L, Colla R, Chiodera P. Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men. Eur J Endocrinol 1994;131:50–5. ISSN 0804–4643 The possible involvement of endogenous opioids in the gamma-aminobutyric acid-controlled (GABAergic) inhibition of growth hormone (GH) and prolactin (PRL) during physical exercise was evaluated in normal men. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. During exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respectively. The administration of naloxone did not modify, whereas sodium valproate significantly reduced the plasma GH and PRL rise during exercise. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was given together with sodium valproate, both GH and PRL responses to exercise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to physical exercise in men. Furthermore, the data argue against a role of naloxone-sensitive endogenous opioids in the control of these hormonal responses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action. Vittorio Coiro, Istituto di Clinica Medica Generale e Terapia Medica, Università di Parma, via Gramsci 14, 43100 Parma, Italy

Mechanisms regulating hormone release and the duration of dioestrus in the lactating rat

1983 ◽  
Vol 99 (2) ◽  
pp. 173-180 ◽  
Author(s):  
S. Hansen ◽  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Dopamine Receptor ◽  
Post Partum ◽  
Prolactin Secretion ◽  
Dopamine Receptor Agonist ◽  
Hormone Release ◽  
Serum Progesterone ◽  
Dopamine Receptor Antagonist ◽  
Lh Secretion ◽  
Cross Fostering ◽  
Prolactin Suppression

Lactation in rats nursing seven pups was associated with a period of dioestrus lasting for 3 weeks, reduced LH secretion, hyperprolactinaemia and increased serum progesterone levels. Removal of the litter resulted in increased LH secretion, a prompt return of oestrus and termination of the prolactin-dependent luteal phase. Administration of domperidone (2·5 mg/day), a dopamine receptor antagonist, to rats deprived of their litters on day 1 or 9 post partum maintained hyperprolactinaemia and delayed the reappearance of oestrus. Administration of bromocriptine (0·5 mg/day), a dopamine receptor agonist, to lactating rats with suckling pups suppressed prolactin secretion and advanced oestrus, females in the middle of lactation being considerably more sensitive to prolactin suppression than those in the early post-partum period. Cross-fostering experiments revealed that the greater sensitivity to bromocriptine of mothers in late lactation was due to their lactational age rather than to the age of the offspring. Similarly, the length of lactational dioestrus was not affected either by giving newborn pups to females in the middle of lactation or by giving 9-day-old pups to newly parturient females.

The inhibitory effect of progesterone on lactogenesis during pregnancy is already evident by mid- to late gestation in rodents

2012 ◽  
Vol 24 (5) ◽  
pp. 704 ◽  
Author(s):  
Constanza M. López-Fontana ◽  
María E. Maselli ◽  
Ana M. Salicioni ◽  
Rubén W. Carón
Keyword(s):  
Mammary Gland ◽  
Hormonal Regulation ◽  
Time Course ◽  
Mammary Epithelium ◽  
Secretory Activity ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Late Gestation ◽  
Pregnant Rats ◽  
Mammary Gland Morphology

Lactogenesis is a very complex process highly dependent on hormonal regulation. In the present study the time-course of the inhibitory actions of progesterone on prolactin secretion, mammary gland morphology and lactogenesis from mid- to late gestation in rodents was investigated. Groups of pregnant rats were luteectomised or administered with mifepristone on Day 10, 13, 15 or 17 of gestation and decapitated 28 or 48 h later. Whole-blood samples and the inguinal mammary glands were taken for determinations of hormone levels and for measurement of mammary content of casein and lactose and for tissue morphology analyses, respectively. Luteectomy or mifepristone evoked prolactin increases only after Day 17 of gestation. Mammary content of casein was increased by both treatments regardless of timing or duration. Mifepristone was less effective than luteectomy in inducing lactose production and the effect was only observed after Day 15 of gestation. Analysis of mammary gland morphology confirmed the observed effect of progesterone on lactogenesis. Both treatments triggered remarkable secretory activity in the mammary gland, even without a parallel epithelial proliferation, demonstrating that the mammary epithelium is able to synthesise milk compounds long before its full lobulo–alveolar development is achieved, provided that progesterone action is abolished. Thus, the present study demonstrates that progesterone is a potent hormonal switch for the prolactin and prolactin-like effects on mammary gland development and its milk-synthesising capacity during pregnancy, and that its inhibitory action is already evident by mid-pregnancy in rodents.

scholarly journals Regulation by endogenous opioids of suckling-induced prolactin secretion in pregnant and lactating rats: role of ovarian steroids

2002 ◽  
Vol 172 (2) ◽  
pp. 255-261 ◽  
Author(s):  
M Soaje ◽  
EG de Di Nasso ◽  
RP Deis
Keyword(s):  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Endogenous Opioids ◽  
Opioid System ◽  
Serum Prolactin ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Subsequent Increase ◽  
Stimulatory Action

Evidence suggests that endogenous opioid peptides are implicated in the suckling-induced prolactin rise. We explored the role of the opioid system and the participation of ovarian hormones in the regulation of prolactin induced by the suckling stimulus at the end of pregnancy in rats with developed maternal behavior, and during lactation. Suckling for 24 h induced a significant increase in serum prolactin on day 19 of pregnancy, which was increased more than three times when naloxone (2 mg/kg s.c.) or mifepristone (2 mg/kg) was administered. The combination of naloxone and mifepristone did not increase serum prolactin more than either compound alone. Administration of tamoxifen (500 microg/kg orally) on days 14 and 15 of pregnancy completely abolished the effect of naloxone, indicating a role for estrogens in establishing this inhibitory role of opioids. To examine the participation of the opioid system during lactation, we used groups of rats on days 1, 3, 5, 12 and 19 postpartum either (i) isolated from the pups for 4 h, or (ii) isolated from the pups for 3.5 h and reunited with them and suckled for 30 min. Naloxone, given just before replacing the pups, prevented the increase in serum prolactin levels observed in the suckled group of rats but had no effect on the basal levels of the isolated rats. To examine whether the participation of the opioid system in the release of prolactin is dependent on the variation of progesterone levels, rats on day 20 of pregnancy were implanted with two cannulae containing progesterone (that blocked postpartum ovulation) or cholesterol, and cesarean surgery was performed on day 21. To maintain lactation, pups (1-3 days old) were replaced every 24 h, and 4 days after the cesarean eight pups were placed in the cage at 1800 h to maintain a strong suckling stimulus during the following 24 h. Naloxone administration significantly reduced serum prolactin levels in control (cholesterol) rats but progesterone implants prevented the inhibitory effect of naloxone and this effect was not modified by treatment with estrogen. These results indicate that the opioid system modulates suckling-induced prolactin secretion, passing from an inhibitory action before delivery to a stimulatory action during lactation. This regulatory shift seems to be dependent on the fall in progesterone concentration at the end of pregnancy and the subsequent increase after the postpartum ovulation and luteal phase.

Luteolytic effect of LH: inhibition of 3β-hydroxysteroid dehydrogenase and stimulation of 20α-hydroxysteroid dehydrogenase luteal activities in late pregnant rats

1996 ◽  
Vol 150 (3) ◽  
pp. 423-429 ◽  
Author(s):  
C O Stocco ◽  
R P Deis
Keyword(s):  
Hydroxysteroid Dehydrogenase ◽  
Good Evidence ◽  
Progressive Decrease ◽  
Control Groups ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Luteal Function ◽  
Treatment Administration ◽  
Stimulation Of

Abstract 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 3β-hydroxysteroid dehydrogenase (3β-HSD) activity, the increase in 20α-hydroxysteroid dehydrogenase (20α-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 μg oLH on day 19 of pregnancy at 0800–0900 h did not modify corpus luteal function 36 h after treatment, but treatment with 4 μg oLH per ovary induced a significant progressive decrease in luteal 3β-HSD activity starting 12 h after treatment, while a significant increase in 20α-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 μg oLH. The intrabursal administration of 8 μg oLH induced an increase in 20α-HSD activity and a decrease in 3β-HSD activity 36 h after treatment. Administration of 4 μg oLH per ovary on day 8 of pregnancy induced a significant increase in serum P4 levels without modifying 3β-HSD activity. In rats treated with oLH on day 19 of pregnancy the decrease in 3β-HSD activity occurred 36 h before the significant increase in 20α-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. Journal of Endocrinology (1996) 150, 423–429

Pregnancy- and lactation-induced changes in active intestinal calcium transport in rats

1992 ◽  
Vol 263 (1) ◽  
pp. G127-G134 ◽  
Author(s):  
A. Boass ◽  
J. A. Lovdal ◽  
S. U. Toverud
Keyword(s):  
Time Course ◽  
Late Pregnancy ◽  
Serum Prolactin ◽  
Marked Rise ◽  
Pregnant Rats ◽  
Ca Transport ◽  
Everted Gut Sac ◽  
Pregnancy And Lactation ◽  
Time Course Study ◽  
Induced Changes

A time course study of active Ca transport in the duodenum and the terminal ileum was conducted using the everted gut sac technique during the last week of pregnancy and throughout lactation. A triphasic pattern was revealed in the proximal duodenum: a marked rise between 18 and 20 days of pregnancy, a plateau maintained during the last 3 days of pregnancy and the first 2-3 days of lactation, and a fall by day 4 of lactation. The late-pregnancy rise was significant also when expressed as milligrams Ca transported relative to tissue weight, indicating that intestinal hypertrophy was not the cause of the increase. The ratio of serosal to mucosal Ca concentration remained low until approximately day 11 of lactation, when it rose toward a new peak. There was no active Ca transport in the ileum until the third week of lactation. Serum prolactin levels increased 10-fold between 18 and 20 days of pregnancy and remained high until at least day 7 of lactation, but did not correlate significantly with duodenal Ca transport. Injected rat prolactin did not result in a precocious rise in Ca transport in pregnant rats. The fluctuations in duodenal Ca transport during lactation were reflected by a small, but statistically significant, decrease in net fractional Ca absorption at 6-9 days compared with either 2-4 days or 13-16 days. We suggest that duodenal active Ca transport plays only a small role in total intestinal Ca absorption in the lactating rat except when dietary Ca is greatly restricted.

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