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PubMed1991

Prolactin responses to vasoactive intestinal polypeptide and thyrotropin releasing hormone in chronic renal failure.

Prolactin response to iv bolus injection of 1 micrograms/kg vasoactive intestinal polypeptide was determined in 8 patients with chronic renal failure undergoing chronic hemodialysis and in 8 normal controls, age- and sex-matched. Plasma prolactin in the patients showed a blunted response following vasoactive intestinal polypeptide injection, whereas the controls showed significantly higher mean peak prolactin value over the baseline value (p less than 0.002). The net rise (peak levels minus basal levels) in plasma prolactin and area under the curve after vasoactive active intestinal polypeptide injection in the controls were significantly greater than those in the patients (p less than 0.001). On a separate day, each individual underwent a TRH (500 micrograms) challenge with the prolactin response determined. The patients had significantly higher peak prolactin values over baseline levels (p less than 0.02) which, however, were not significantly different from those in the control group. In the patients, the peak net prolactin increments and area under the curve were significantly higher following TRH than following vasoactive intestinal polypeptide (p less than 0.05). The net prolactin increments to TRH challenge were significantly higher in the control group than in the patients (p less than 0.001). The results demonstrate the blunted prolactin response to the stimulatory effect of vasoactive intestinal polypeptide and TRH in chronic renal failure. In chronic renal failure prolactin release after vasoactive intestinal polypeptide is more blunted than after TRH. These data suggest that the responsiveness of plasma prolactin to vasoactive intestinal polypeptide is defective in these patients, though the mechanism(s) are yet to be defined.

Adult↗
PubMed1988

Serum concentrations of prolactin, oestrogen and LH during the perioestrous period in prepubertal gilts induced to ovulate and mature gilts.

The temporal relationships of serum prolactin, oestrogen and LH concentrations during the perioestrous period were compared in prepubertal gilts induced to ovulate by PMSG and hCG and in mature gilts. In Exp. 1, 2 sustained prolactin surges, beginning 4 days and 1 day before the preovulatory LH surge, occurred in all mature gilts. A single preovulatory prolactin surge occurred in 3 prepubertal gilts, starting just before the preovulatory LH surge, but 4 prepubertal gilts had neither a prolactin nor an LH surge. A status (prepubertal or mature) versus time interaction (P less than 0.01) was detected for serum prolactin concentrations. A preovulatory oestrogen surge occurred in all gilts but was of lesser magnitude (P less than 0.01) and duration (P less than 0.05) in the prepubertal gilts without prolactin and LH surges compared to mature gilts and of lesser magnitude (P less than 0.01) compared to prepubertal gilts with prolactin and LH surges. The relative timing of the oestrogen surge in prepubertal gilts corresponded with that of mature gilts when adjusted to the LH surge (if present) but was delayed (P less than 0.01) in all prepubertal gilts if standardized to the hCG injection. In Exp. 2, mature gilts were examined to determine whether 2 perioestrous prolactin surges were characteristic of all cycling gilts. Of 9 gilts, 8 exhibited an initial prolactin surge 4-5 days before oestrus and 5/9 gilts exhibited a periovulatory prolactin surge. The presence of 2 perioestrous serum prolactin surges was not a requirement for subsequent pregnancy maintenance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Annual changes in serum concentrations of prolactin in captive male black bears (Ursus americanus).

Prolactin may be involved in the regulation of reproduction in black bears (Ursus americanus) as it is a mediator of photoperiodic changes in a number of species. The objectives of this study were to validate a radioimmunoassay to measure prolactin in bear serum and to describe seasonal changes in serum prolactin concentrations in captive male bears. Serum samples were obtained nine times during a year from three captive male black bears that were denning between November and March and active during the other months. The heterologous prolactin radioimmunoassay, using pig 125I-labelled prolactin and goat anti-pig prolactin as a primary antibody, was validated. Injection of thyrotrophin-releasing hormone into the three male bears in June resulted in a rapid increase in serum concentrations of prolactin (t = 0, 11.4-14.8 ng ml-1; t = 15-30 min, 18.4-28.7 ng ml-1). The sensitivity of the assay was 0.08 ng per tube. Intra- and interassay coefficients of variation were 5.5% (n = 6) and 5.7% (n = 6), respectively. Serum concentrations of prolactin changed seasonally, with the lowest concentrations in December (mean +/- SD = 1.1 +/- 0.1 ng ml-1); this was followed by a gradual increase between January (2.6 +/- 0.6 ng ml-1) and April (6.4 +/- 1.2 ng ml-1) and the highest concentrations in May (17.6 +/- 4.7 ng ml-1), preceding peak testosterone concentrations in June. The observation that prolactin secretion increased with increasing daylength suggests that photoperiod may be an external regulator. The presence of high concentrations of prolactin before peak testosterone concentrations suggests that prolactin may play a role in regulating seasonal changes in the testes.

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↗
PubMed1991

Localization of the sites of synthesis and action of prolactin by immunocytochemistry and in-situ hybridization within the human utero-placental unit.

While the fetal pituitary synthesizes and releases prolactin, it is also produced within the utero-placental unit during pregnancy in women and has been localized in the amnion, chorion and decidua. However, it is not clear whether prolactin is synthesized within all these non-fetal pituitary tissues. We have investigated prolactin production and its gene expression using tissue culture, immunocytochemistry and in-situ hybridization techniques. Prolactin was immunolocalized not only in the decidua but also in amnion and trophoblast cells. In contrast, the in-situ hybridization results showed that silver grains, formed by specific hybridization of a prolactin cDNA probe to prolactin mRNA, were confined to decidual cells of early and term pregnancy. The results from tissue cultures correlated well with those of in-situ hybridization, that is that only the decidua made detectable prolactin, while it was undetectable in the culture medium from trophoblast tissue, irrespective of the stage of pregnancy. This study, for the first time, establishes that only decidualized cells are involved in biosynthesis of prolactin; other prolactin-containing cells in the amnion and trophoblast appear to sequester prolactin, possibly via receptors, suggesting that prolactin may play an important paracrine role within the amnion and syncitio- and cytotrophoblast of the utero-placental unit.

Blotting, Northern↗
PubMed1977

Influence of restraint on plasma prolactin and corticosterone in female rats.

The effect of restraint on plasma prolactin and corticosterone concentrations was investigated in chronically catheterized, ovariectomized (OVX) or ovariectomized, oestrogen-treated (OVX-PEP) rats. Restraint was induced by tying the hind legs together. In OVX rats, prolactin levels were unchanged following restraint, either during the morning (10.00 h) or afternoon (14.00 h). Prolactin levels increased in OVX-PEP animals when restraint was initiated in the morning; when restraint was initiated in the afternoon the prolactin response depended upon the level of prolactin before restraint. If levels were low (pre-surge) the response to restraint was similar to that observed in the morning; if prolactin levels were high (surge) the response to restraint was reversed and the prolactin level declined. The morning prolactin response to restraint was significantly inhibited and the afternoon surge was retarded in adrenalectomized OVX-PEP (OVX-PEP-ADX) rats; however, in OVX-PEP animals maintained on 0-9% NaCl drinking solution, the morning prolactin response to restraint was also blunted, although the afternoon surge was normal. In OVX-PEP-ADX animals injected with either vehicle alone, or 2 or 4 mg corticosterone for 4 days, and sampled on the morning of day 5, the prolactin response to restraint was absent. Furthermore, when OVX-PEP animals were injected daily with either vehicle or 4 mg corticosterone/day, they showed no increase in prolactin in response to restraint when values were compared with those of uninjected animals. Corticosterone levels after restraint were higher than initial values in all of the above experimental conditions.

Adrenalectomy↗
PubMed1978

DNA synthesis and depletion of prolactin in the pituitary gland of the male rat.

Haloperidol, bromocriptine and diethylstilboestrol dipropionate were given in various régimes to male rats to determine their effects on pituitary DNA synthesis, prolactin secretion and growth hormone secretion. Haloperidol increased serum prolactin but did not stimulate pituitary DNA synthesis or reduce pituitary prolactin concentrations. Haloperidol potentiated the effects of oestrogen on serum prolactin and on pituitary DNA synthesis; pituitary prolactin concentrations were greatly reduced, and growth hormone secretion was slightly inhibited. The inhibitory effects of bromocriptine in oestrogen-stimulated rats were demonstrated by smaller pituitary weights and decreased DNA synthesis; serum prolactin levels were lowered and pituitary prolactin concentrations were increased. Haloperidol, given to rats treated with oestrogen and bromocriptine, reversed the inhibitory effects of bromocriptine on DNA synthesis and serum prolactin; pituitary prolactin concentrations fell to well below normal. The results suggest that the haloperidol potentiation of oestrogen-induced pituitary DNA synthesis may depend upon stimulation of prolactin secretion together with reduction of intracellular prolactin levels.

Animals↗
PubMed1978

Transfer of milk prolactin to the plasma of neonatal rats by intestinal absorption.

Prolactin passes from the systemic circulation of lactating rats into the milk where it can be consumed by the young rats during suckling. 131I-Labelled rat prolactin was detected in the plasma of 9- to 14-day-old rats after being nursed by mothers previously injected with 131I-labelled rat prolactin and after the pups had received 131I-labelled rat prolactin by gastric intubation. It was estimated that 16% of the 131I-labelled rat prolactin given by gastric intubation subsequently appeared in the plasma of the neonate. Gastric administration of 10.5 or 21.0 microgram B-1 rat prolactin significantly raised the level of prolactin in the plasma of 13-day-old pups, but a similar increase was not observed when 27-day-old rats were given 46.2 microgram B-1 prolactin by gastric intubation. The concentration of prolactin in the plasma of 13- to 14-day-old rats rose to 55 ng/ml 30 min after the onset of nursing by mothers whose mammary glands were full of milk, whereas the concentration in the plasma of offspring suckled by mothers with empty mammary glands remained at basal values. It is concluded that the intestine of the newborn rat is permeable to prolactin and that milk may constitute an exogenous source of prolactin for the suckled offspring.

Animals↗
PubMed1979

Synthesis of prolactin by human decidua in vitro.

To determine whether human decidua and/or chorion synthesizes and secretes prolactin, explants of decidua obtained at Caesarian section and explants of chorion from the membranes separating dizygotic twins were cultured for periods of up to 6 days. The decidual explants released 366 +/- 37 ng prolactin/100 mg tissue (mean +/- S.D.) during each day in culture and incorporated 3H-labelled amino acids into immunoprecipitable prolactin. In the radioimmunoassay for prolactin, serial dilutions of incubation medium displaced 125I-labelled prolactin parallel to the displacement by pituitary prolactin and the prolactin in the medium eluted from Sephadex G-150 in a position indentical to that of pituitary prolactin. Chorionic explants released prolactin into the incubation medium during day 1 of culture only and did not incorporate 3H-labelled amino acids into prolactin. These results demonstrate that prolactin is synthesized by the decidua and not by the chorion and suggest that the decidua is the source of prolactin in amniotic fluid.

Amino Acids↗
PubMed1979

Failure of melatonin to increase serum prolactin levels in ovariectomized rats subjected to superior cervical ganglionectomy or pinelaectomy.

The effects of melatonin on serum prolactin levels were examined in ovariectomized rats primed with oestradiol and progesterone, and subjected to bilateral superior cervical ganglionectomy or pinealectomy. Ganglionectomy resulted in a significant depression of the serum prolactin concentrations, as well as in impairment of the prolactin release evoked by administration of steroid. Treatment with melatonin increased serum prolactin in control but not in ganglionectomized rats. Injection of melatonin protentiated the steroid-induced release of prolactin in control rats; this effect of melatonin was not detected in ganglionectomized rats. Pinealectomy did not affect basal prolactin levels, nor impair the release of prolactin evoked by steroid treatment; however, it was effective in blocking the melatonin-induced release of prolactin in vehicle-treated rats, as well as the potentiation of steroid-induced prolactin release by melatonin. Intracranial surgery by itself increased prolactin release. These results suggest that systemically administered melatonin needs an intact pineal gland to augment serum prolactin levels.

Animals↗
PubMed1985

Contrasting effects of prolactin on luteal and follicular steroidogenesis.

To determine whether prolactin affects both luteal and follicular production of testosterone and oestradiol, pseudopregnant rats, either intact or hypophysectomized on day 8, were injected daily between days 8 and 9 with 1.5 i.u. human chorionic gonadotrophin (hCG), 250 micrograms prolactin or a combination of both. Control rats were given vehicle. On day 9, blood was obtained from the ovarian vein and corpora lutea and follicles were isolated and incubated in vitro for 2 h. Administration of hCG to intact rats increased ovarian secretion of testosterone and oestradiol dramatically, but did not affect progesterone secretion. Hypophysectomy on day 8 of pseudopregnancy was followed by a drop in ovarian steroid secretion. Prolactin treatment of hypophysectomized rats markedly enhanced progesterone production but had no stimulatory effect on either testosterone or oestradiol. In contrast, hCG dramatically enhanced ovarian secretion of both testosterone and oestradiol without affecting progesterone secretion. Prolactin administered together with hCG antagonized the stimulation of both testosterone and oestradiol secretion by hCG, yet increased progesterone production. When the specific effects of hCG and prolactin administration on follicles and corpora lutea were studied separately, it was found that hCG treatment in vivo greatly stimulated testosterone and oestradiol production by both tissues in vitro. Since hCG only marginally affected aromatase activity in the follicle, had no effect on aromatase activity in luteal cells and did not increase progesterone synthesis, it appears that hCG acts to increase the formation of androgen substrate for oestradiol biosynthesis. Prolactin, administered with or without hCG, inhibited both basal and hCG-stimulated testosterone and oestradiol synthesis by the follicle. In sharp contrast to its inhibitory effect on follicular production of steroids, prolactin appears to be essential for LH stimulation of testosterone and oestradiol by the corpus luteum. In the absence of prolactin, luteal cells gradually ceased to respond to LH and decreased their output of testosterone and oestradiol. Prolactin administration to hypophysectomized rats did not affect luteal cell production of either steroid. However, corpora lutea of rats treated with prolactin responded to the hCG challenge with an increase in testosterone and oestradiol synthesis. In summary, results of this investigation demonstrate that prolactin affects follicular and luteal production of testosterone and oestradiol in opposite ways.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Behavioural and physiological effects of prolactin in incubating ring doves.

The role of prolactin in the maintenance of incubation behaviour in ring doves was re-examined and the dose-response relationships for behavioural, target tissue and body weight changes induced by injections of prolactin were compared in doves tested during the incubation phase of the breeding cycle. Doves given injections of prolactin twice a day starting on day 4 of incubation, during a 10-day period of isolation from their mates and nests, showed a higher persistence of incubation behaviour than doves injected with saline vehicle. However, the prolactin treatment failed to maintain incubation behaviour to the same extent as that observed in non-isolated untreated breeding pairs. Liver and body weights were higher and testicular weights lower in birds treated with high doses of prolactin than in non-isolated birds which had been incubating for 14 days. Good dose-response relationships were established between body, liver, crop and testes weights and the dose of prolactin administered. However, only a weak dose-response relationship was observed between prolactin and the maintenance of incubation behaviour. Overall, females injected with prolactin displayed more quiet sitting behaviour, less body weight gain and more gonadal regression than males injected with prolactin. Males in untreated breeding pairs had higher liver weights and lower crop weights than females. It is concluded that prolactin plays a role in maintaining readiness to incubate in doves, but that other factors may also contribute to this response. Further, it appears that prolactin mediates several target tissue changes which are sex-specific during incubation.

Animals↗
PubMed1986

Effects of lactation and season on plasma prolactin concentrations and response to bromocriptine during lactation in the Bennett's wallaby (Macropus rufogriseus rufogriseus).

Prolactin concentration was measured in plasma collected each week for 13 months from lactating and non-lactating Bennett's wallabies (Macropus rufogriseus rufogriseus). In non-lactating animals, prolactin concentrations decreased towards the end of the study but such changes did not appear to fit a seasonal pattern. Prolactin concentrations were low during early lactation and at a similar level to non-lactating animals, increased significantly during late pouch life (February-May), and then returned to non-lactating levels at a time coincident with permanent exit of the joey from the pouch. Temporary removal of joeys from their mothers in April was followed by a rapid decline in prolactin concentrations which remained low for 24 h until the joey was returned to its mother, whereupon prolactin concentrations increased significantly within 2 h. The effect of a single injection of bromocriptine (5 mg/kg) on lactation, embryonic diapause and plasma prolactin concentrations was examined at two stages of lactation. In November (lactational diapause), bromocriptine had no effect on prolactin concentrations but two out of four suckling joeys died on days 13 and 14 after treatment, and three out of four females gave birth on days 27, 27 and 28. Bromocriptine treatment in April (seasonal diapause) was followed by a significant reduction in prolactin concentrations and reduced growth rate of joeys belonging to treated females. New births were not observed. In view of the effect of bromocriptine on plasma prolactin concentrations in late lactation and the demonstration that domperidone (a dopamine antagonist) significantly increases plasma prolactin concentrations, it would seem that dopamine can act as a prolactin inhibitory hormone in this as in other mammalian species.

Animals↗
PubMed1986

Factors affecting prolactin secretion during the breeding cycle of the ring dove (Streptopelia risoria) and its possible role in incubation.

Plasma prolactin began to increase significantly about 5 days after the onset of incubation in both sexes of the dove to reach a peak at the time of hatch. At this time, the concentration of prolactin in the plasma of the female was significantly higher than in the male. In the middle of the incubation period prolactin levels measured over a 24-h period remained constant in both sexes, although the male sits during the middle of the day and the female for the rest of the time. Nest deprivation resulted in a sharp, significant decline in the concentration of prolactin in both sexes. Newly hatched squabs stimulated the release of prolactin only in those doves which had been incubating eggs for several days. A distinct sex difference was observed in the expression of nest defence behaviour of the ring dove during the breeding cycle. At the time of laying, the female was significantly more aggressive than the male and her aggression increased only slightly up to the time of hatching. In contrast, male aggression increased gradually from a low level at laying to reach a peak at the time of hatching. The levels of plasma progesterone in the female showed a significant increase around the time of lay. No significant changes occurred in the plasma concentration of either progesterone or 17 alpha-hydroxyprogesterone in the male. Administration of prolactin increased the length of time of incubation of infertile eggs. Nest manipulations which had the effect of inducing the doves to begin incubation 4 days before laying showed that (1) the length of time of incubation of infertile eggs is fixed and independent of events which occur at courtship or oviposition, (2) the initiation of the increase in plasma prolactin concentration during incubation is independent of events which occur at courtship and oviposition and (3) the termination of incubation is always preceded by a fall in the concentration of plasma prolactin. It is concluded that the length of time of incubation is dependent upon sustained raised levels of plasma prolactin. The concentration of plasma prolactin increases several days after the onset of incubation in response to the tactile stimulation of sitting. High levels, if maintained by visual stimulation from the nest, maintain incubation for a fixed period. After this, if the eggs fail to hatch, prolactin levels fall and the doves cease incubation and begin a new cycle.

Animals↗
PubMed1986

Transient increase in prolactin secretion following hypothalamo-pituitary disconnection in ewes during anoestrus and the breeding season.

Hypothalamic control of prolactin secretion was studied in ovariectomized ewes by comparing the effects of hypothalamo-pituitary disconnection (HPD) and sham-operation (sham-HPD). HPD caused a two-fold increase in plasma prolactin concentrations on days 1 and 7 following surgery during anoestrus and a tenfold increase during the breeding season. Thereafter, concentrations gradually declined to be similar to those in sham-HPD ewes by day 43 (breeding season) and day 145 (anoestrus). The maximum plasma prolactin response to HPD was similar during the two seasons (anoestrus: 128 +/- 15 bs breeding season: 118 +/- 13 micrograms/l). Sham-HPD had no effect on plasma prolactin concentrations. Prolactin pulse frequency was not affected by HPD, but increases in plasma prolactin concentrations were associated with increases in pulse amplitude. At the time of the normal anoestrus, plasma prolactin concentrations rose in both the HPD and sham-HPD ewes, raising the question of extra-hypothalamic regulation of seasonal changes in prolactin secretion. Plasma LH and FSH concentrations became undetectable in HPD ewes but were unaltered in sham-HPD ewes. We conclude that hypothalamic inhibition of pituitary prolactin secretion in the sheep can be demonstrated by HPD but that this effect is not sustained. This transience may indicate the additional requirement of hypothalamic-releasing factors in the control of prolactin release. In addition, the surgically isolated ovine pituitary of the HPD animal has an inherent pulsatile secretion of prolactin.

Anestrus↗
PubMed1987

A possible dual regulation of prolactin release by the serotoninergic system in rats at pro-oestrus and during late pregnancy: role of ovarian hormones.

The effect of para-chlorophenylalanine (pCPA), an inhibitor of serotonin synthesis, on prolactin release was studied in rats on the day of pro-oestrus and at the end of pregnancy (day 19). The surges of prolactin normally seen in the afternoon of pro-oestrus in intact rats and in rats ovariectomized on dioestrous day 2 and primed with oestrogen were significantly inhibited by pCPA treatment. Administration of 5-hydroxytryptophan reversed the inhibitory action of pCPA on prolactin release. Treatment with progesterone also completely reversed the inhibitory effect of pCPA on prolactin release in pro-oestrous rats and partially reversed it in ovariectomized oestrogen-treated rats. Ovariectomy on day 19 of pregnancy induced a significant release of prolactin 12 and 24 h later. Administration of pCPA on day 18 of pregnancy produced a marked increase in serum concentrations of prolactin on days 19 and 20 in rats left intact or ovariectomized on day 19. Administration of 5-hydroxytryptophan significantly reversed this stimulatory effect of pCPA on prolactin release but did not modify the release of prolactin induced by ovariectomy. Methiothepin (1-[10,11-dihydro-8-(methylthio) less than b,f greater than thiepin-10,41]-4-methylpiperazine maleate), a serotonin receptor blocker, also induced a significant increase in serum concentrations of prolactin on day 20 of pregnancy in rats left intact or ovariectomized on day 19. These results suggest the existence of different serotoninergic actions in the regulation of prolactin release at pro-oestrus and in late pregnancy. Serotonin facilitates the surges of serum prolactin released at pro-oestrus and in ovariectomized rats treated with oestrogen; progesterone enhances this effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

In-vitro effects of mammalian and amphibian prolactins on hepatic vitellogenin synthesis in Rana esculenta.

Male and female Rana esculenta liver was induced in an in-vitro system by homologous and Rana catesbeiana pituitary to synthesize and release vitellogenin, a lipoglycophosphoprotein precursor of yolk proteins, lipovitellins and phosvitins, in oviparous vertebrates. In the present experiments, the action of prolactin on hepatic vitellogenin synthesis and release was investigated, using ovine prolactin and Rana catesbeiana prolactin. The effects of prolactin on hepatic vitellogenin synthesis displayed different trends related to sex; male liver was found to be more responsive than female liver to both ovine and frog prolactin; more-over, the response to prolactin was dose-related (r = 0.998; P < 0.05) in male but not in female liver. In both sexes, a high degree of seasonality in the responsiveness of the liver was found, since the vitellogenin levels induced by prolactin during the winter phase were significantly (P < 0.001) higher than those produced during the summer phase. Thus, there was no significant difference between the action of ovine and frog prolactin on vitellogenin synthesis; in fact, mammalian prolactins are structurally similar with regard to nucleotide and amino acid sequences. The direct action of prolactin on hepatic vitellogenin synthesis in the frog Rana esculenta is discussed, on the basis of the role played by prolactin as an important growth modulatory hormone in fetal and adult tissues.

Animals↗
PubMed1987

Effects of physiologic and pharmacologic agents on serum prolactin concentrations in the nonpregnant mare.

Four studies were conducted to evaluate the effects of several physiologic and pharmacologic agents on serum prolactin concentrations in the nonpregnant mare. An increase in prolactin measured in response to administration of thyrotropin-releasing hormone (TRH; 50 micrograms, iv) was found not to vary (P = .20) in mares in estrus compared with mares in diestrus (5 to 10 d post-ovulation). Administration in the dopamine receptor blocker, metoclopramide (25 or 100 mg, im), rapidly increased serum prolactin, and the response was dependent on dose administered (total prolactin measured for 420 min was 3,362.7 +/- 182.1 ng for 25 mg, and 4,485.7 +/- 212.6 ng for 100 mg administered im; P less than .05), but not on route of injection (3,026.3 +/- 492.3 ng prolactin with 25 mg, iv; P less than .05). Similarly, sulpiride, a D-2 dopamine receptor blocker, induced an increase in serum prolactin, which appeared to be maximal at a dose of 25 mg (6,556.3 +/- 636.9 ng prolactin/420 min compared with 6,594.5 +/- 169.3 ng prolactin/420 min with 100 mg sulpiride; P less than .10). Finally, bromocriptine, a dopamine agonist, decreased serum prolactin compared with vehicle-injected controls, but the inhibitory effect was found only when basal levels of serum prolactin were highest (in May). These data suggest that mechanisms controlling prolactin secretion in the mare are similar to those described in other mammalian species, and that the seasonal decline in serum prolactin is not the result of increased sensitivity to the proposed prolactin-inhibiting factor, dopamine.

Animals↗