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PubMed2004

Melatonin blocks inhibitory effects of prolactin on photoperiodic induction of gain in body mass, testicular growth and feather regeneration in the migratory male redheaded bunting (Emberiza bruniceps).

Little is known about how hormones interact in the photoperiodic induction of seasonal responses in birds. In this study, two experiments determined if the treatment with melatonin altered inhibitory effects of prolactin on photoperiodic induction of seasonal responses in the Palearctic-Indian migratory male redheaded bunting Emberiza bruniceps. Each experiment employed three groups (N = 6-7 each) of photosensitive birds that were held under 8 hours light: 16 hours darkness (8L:16D) since early March. In the experiment 1, beginning in mid June 2001, birds were exposed to natural day lengths (NDL) at 27 degree North (day length = ca.13.8 h, sunrise to sunset) for 23 days. In the experiment 2, beginning in early April 2002, birds were exposed to 14L:10D for 22 days. Beginning on day 4 of NDL or day 1 of 14L:10D, they received 10 (experiment 1) or 13 (experiment 2) daily injections of both melatonin and prolactin (group 1) or prolactin alone (group 2) at a dose of 20 microgram per bird per day in 200 microliter of vehicle. Controls (group 3) received similar volume of vehicle. Thereafter, birds were left uninjected for the next 10 (experiment 1) or 9 days (experiment 2). All injections except those of melatonin were made at the zeitgeber time 10 (ZT 0 = time of sunrise, experiment 1; time of lights on, experiment 2); melatonin was injected at ZT 9.5 and thus 0.5 h before prolactin. Observations were recorded on changes in body mass, testicular growth and feather regeneration. Under NDL (experiment 1), testis growth in birds that received melatonin 0.5 h prior to prolactin (group 1) was significantly greater (P < 0.05, Student Newman-Keuls test) than in those birds that received prolactin alone (group 2) or vehicle (group 3). Although mean body mass of three groups were not significantly different at the end of the experiment, the regeneration of papillae was dramatically delayed in prolactin only treated group 2 birds. Similarly, under 14L:10D (experiment 2) testes of birds receiving melatonin plus prolactin (group 1) and vehicle (group 3) were significantly larger (P < 0.05, Student Newman-Keuls test) than those receiving prolactin alone (group 2). Also, birds of groups 1 and 3, but not of group 2, had significant (P < 0.05, 1-way repeated measures Analysis of Variance) gain in body mass. However, unlike in the experiment 1, the feather regeneration in birds of the three groups was not dramatically different; a relatively slower rate of papillae emergence was however noticed in group 2 birds. Considered together, these results show that a prior treatment with melatonin blocks prolactin-induced suppression of photoperiodic induction in the redheaded bunting, and suggest an indirect role of melatonin in the regulation of seasonal responses of birds.

Animals↗
PubMed1981

Opioid regulation of prolactin secretion: evidence for a specific role of beta-endorphin.

Previous studies have shown that exogenously administered opioids, including beta-endorphin, stimulate prolactin release. The fact that naloxone has been shown to lower baseline and stress-induced serum prolactin in rats suggests that endogenous opioids may participate in prolactin regulation, but does not specify which opioid is involved. In a previous study we showed that intravenously administered anti-beta-endorphin antiserum had no effect on either baseline or stress-induced prolactin release in rats. In the present study we have repeated our earlier experiments, but have given the antiserum into the cerebral ventricles rather than intravenously. Significant lowering of baseline serum prolactin, to 56.6% +/- 10.6% (SEM) that of controls (p less than 0.005), was noted. Also noted was blunting of the stress-induced prolactin rise, to 69.2% +/- 6.7% that of controls (p less than 0.002). These results indicate that beta-endorphin is specifically involved in both the tonic and stress-mediated release of prolactin. Because the magnitude of prolactin lowering with antiserum was at least as great as what we had earlier observed with naloxone, they suggest that beta-endorphin is the major and possibly the sole opioid involved in prolactin regulation. They also indicate that the previous lack of effect of anti-beta-endorphin antiserum on serum prolactin was due to its failure, after intravenous administration, to achieve effective concentration at critical controlling sites within the brain.

Animals↗
PubMed1975

The influence of adrenergic, dopaminergic, cholinergic and serotoninergic drugs on plasma prolactin levels in ovariectomized, estrogen-treated rats.

Levels of plasma prolactin were estimated in ovariectomized, estrogen-treated rats following the systemic administration of several neural blocking and stimulating drugs. Phenoxybenzamine, an alpha-adrenergic blocker, at high doses, increased plasma prolactin. Phenotlamine, another alpha-adrenergic blocker, and propranolol, a beta-adrenergic blocker, also increased prolactin but the responses were small and transient. Clonidine, an alpha-adrenergic stimulating drug, elevated prolactin levels whereas the beta-adrenergic stimulator isoproterenol had no effect. Dopaminergic blockade by pimozide increased levels of prolactin while stimulation of dopamine receptors by apomorphine decreased prolactin release. Atropine (a muscarinic chilinergic blocker), arecoline (a muscarinic stimulator) and nicotine (a nicotinic cholinergic stimulating drug) did not affect basal prolactin levels. Mecamylamine (a nicotinic blocker) produced a small transient elevation in plasma prolactin. Methiothepin, an alleged serotoninergic blocker, markedly increased prolactin secretion, as did serotonin. The data suggested the involvement of several neurotransmitters in the control of basal secretion of prolactin.

Adrenergic alpha-Antagonists↗
PubMed1975

Effects of porcine hypothalamic extract on prolactin release in the rat.

The effect of crude extract of porcine stalk-medium eminence (SME) on release of prolactin, measured by radioimmunoassay, has been studied in the rat. In male rats, intravenous administration of 3-4 SME equivalents caused an acute increase in serum prolactin levels. This prolactin-releasing factor (PRF) effect was observed in rats anesthetized with either pentobarbital or ether, and was not dependent upon estrogen pretreatment of the animals. Prolactin release was not seen with doses of 5 or 50 mug of synthetic thyrotropin-releasing hormone (TRH). The presence of porcine SME extract enhanced the release of prolactin by male rat pituitary halves incubated for 2 h in Medium 199. This effect was observed whether or not pituitary donors were pretreated with estrogen. In contrast to the observations in male animals, administration of 3 porcine SME equivalents to lactating rats separated from their litters for 4 h did not elevate serum prolactin. Failure to observe PRF activity could not be accounted for by the anesthetic employed. In vitro, porcine SME extract did not stimulate release of prolactin by pituitaries from lactating rats. Intraperitoneal injection of extract of 3 porcine SME equivalents inhibited the increase in serum prolactin which occurs when lactating rats are reunited with their litters for 30 min after 4 h of separation. These results are consistent with the concept that suckling-induced prolactin release is accomplished by cessation of discharge of a prolactin release-inhibiting factor (PIF). Furthermore, since effects of PRF were observed only in male rats, it is also concluded that the physiological state of animals treated with hypothalamic extracts is an important factor in determining responsiveness to either PIF or PRF.

Animals↗
PubMed1975

Human and monkey prolactin and growth hormone: separation of polymorphic forms by isoelectric focusing.

The feasibility of using isoelectric focusing for the separation of primate pituitary growth hormone from prolactin and for the characterization of polymorphic forms of these hormones was explored. In a pH 3--10 gradient, extracts of both human and cynomolgus monkey pituitaries were each resolved into 4 growth hormone components and at least 3 prolactin components, as shown by radioimmunoassay. In narrower gradients (of 2--3 pH units) greater resolution was achieved; the principal growth hormone components were well separated from the principal prolactin components but there was overlapping of some minor components. A partially purified human prolactin preparation was found to contain 4 prolactin components, one of which had a prolactin/growth hormone ratio of 760. Clinical grade human growth hormone was also resolved into at least 5 prolactin and 5 growth hormone components, many of which had higher pI values than those found in pituitary extract. Under the conditions used, both growth hormone and prolactin were found to be polymorphic with respect to isoelectric point. Some of the human prolactin components were found to contain less than 0.2% growth hormone by radioimmunoassay. Monkey growth hormone containing 0.01% prolactin was isolated. These findings demonstrate that isoelectric focusing is useful for the preparation of both growth hormone and prolactin which are essentially free of one another. Furthermore, the polymorphic forms were repeatedly found in preparations obtained by several methods and from 2 different species, suggesting that these forms are not artifacts.

Animals↗
PubMed1975

[Prolactin releasing action of the hypothalamic extract in last stage of pregnant rats (author's transl)].

Regulation of prolactin secretion in pituitary is considered to be mostly carried with the action of prolactin inhibiting factor in hypothalamus. We have investigated on the subject of prolactin releasing factor in the hypothalamus of rats in last stage of pregnancy using puerperal and ovariectomized rats as recipients. After prepared the cell-free system of pregnant rat hypothalamus with sonic oscillator, supernatant was produced by ultracentrifuge (25,000 X g, 30 min.) and utilized for the experiments. When the extract was injected intramuscularly to puerperal rats (48-60 hours after delivery), serum prolactin values increased gradually to 3 times of control values, but pituitary prolactin values showed the variation with decrease and recovery. The control values were obtained by determination after injection of cerebral cortical extract to puerperal rats. After administration of a extract of non-pregnant rat hypothalamus to puerperal rats, serum prolactin values decreased and pituitary prolactin values increased antagonistically. In the ovariectomized rats pretreated with estradiol and progesterone, serum prolactin values increased in 1 hour after administration of the extract of pregnant rat hypothalamus, but pituitary prolactin values did not show any variation. The present experiment suggests that the prolactin secretion promoting factor exists in the hypothalamus of pregnant rats and predominates over as compared with PIF in last stage of pregnancy.

Animals↗
PubMed1981

[The control of prolactin surge by ovarian steroids in the early phase of pseudopregnancy in rats (author's transl)].

The secretory patterns of prolactin and progesterone and the participation of ovarian steroids for their secretion in the early phases of delayed-pseudopregnancy (D-PSP) were studied in rats. D-DSP or immediate pseudopregnancy (I-PSP) was induced by vaginal stimulation (VS) given at 14:00 on diestrus 2. Blood for prolactin and progesterone analyses was obtained by decapitation performed every 2 hours between 13:00 on diestrus 2 and 13:00 on proestrus of the estrous cycle and during the corresponding stages of PSP. After the VS given on diestrus 2, concentrations of plasma prolactin and progesterone in D-PSP rats were the same as those of normal cyclic rats. In the rats given VS on estrus (Day 0) to produce I-PSP, a nocturnal surge of prolactin was obvious in the morning of Day 3. Plasma progesterone levels were also high in these rats. However, in the ovariectomized-adrenalectomized (OVX-ADX) rats, on which the operation was performed at various stages of the estrous cycle, a nocturnal surge of prolactin was clearly observed after the VS given at 14:00 on diestrus 2. The appearance of a nocturnal prolactin surge by the VS in the OVX-ADX rats was inhibited by the administration of estradiol-17 beta (1 microgram/rat). The nocturnal surge of prolactin in the early phase of I-PSP was also diminished by the administration of the steroid. Concomitant administration of progesterone with estrogen, however, overcame the inhibition of the nocturnal surge of prolactin by estrogen. These results indicate that the stabbing secretion of prolactin observed in the early phases of pregnancy or pseudopregnancy is modulated by the ovarian steroids and also suggests that the increasing secretion of estrogen from diestrus 2 to proestrus in the normal estrous cycle suppresses the prolactin surge expected by VS and resulting in D-PSP.

Animals↗
PubMed1976

Effect of age and sex on circulating and pituitary prolactin levels in human.

In an attempt to determine whether age or sex affects prolactin secretion in the human, basal levels of serum prolactin, and its response to TRH administration as well as the pituitary content of this hormone were compared between both sexes and among the different agent groups. In 315 adult subjects of various ages, the mean basal levels of prolactin were found to be higher in women than in men of the same age groups with the exception of the sixth decade. The effect of age on serum prolactin concentrations, on the other hand, was not demonstrated. Similarly, the prolactin response to intravenous injections of 500 mug of TRH was significantly greater in female subjects than in males of both young and aged groups. No relationship between the prolactin response and the day of menstrual cycle in young women was apparent. Although quantitative difference in TRH-induced prolactin release was not observed between young and elderly subjects, the occurrence of prolactin peak and the elimination of the circulating prolactin following TRH administration were delayed in the aged groups. Taken together with the demonstration of a higher content of this hormone in female pituitary glands compared with those of males, it was concluded that prolactin secretion is enhanced in female subjects throughout life after puberty and that aging, per se, is not associated with an alteration in the rate of secretion of this hormone in human subjects.

Adolescent↗
PubMed1983

Prolactin release induced by stress and the influence of oestrogen and progesterone treatments, sex and daily rhythm.

The effect of sex, ovarian steroids and time of the day on the release of prolactin induced by stress was studied. Albino rats were bled by heart puncture and immediately anaesthetized with ether; 10 min later they were bled again. Ovariectomized, oestrogen-primed rats showed a daily rhythm in the stress (bleeding plus ether) induced prolactin release with maximal concentration of prolactin in the serum at night (01.00 h) and minimum in the morning (09.00 h). IN ovariectomized, oestrogen-treated rats the rise of prolactin in the serum after stress was higher than in the non-treated rats both in the morning and at night. However in the afternoon (17.00 h), when the pre-stress levels of prolactin were high, the response to stress was reversed and prolactin levels declined. A similar effect was seen in the ovariectomized, oestrogen-primed rats 4 h after the injection of progesterone. In these animals the concentration of prolactin in serum was high and declined after stress. However 28 h after injection of progesterone stress failed to induce any change in prolactin release. Progesterone injected into ovariectomized, non-primed rats did not influence the response to stress. In male rats, both intact and castrated, the increase of prolactin concentration in serum after stress was lower than in females and failed to exhibit a circadian rhythm. These results show the importance of the hormonal background and the time of the day in the magnitude of prolactin release induced by stress.

Animals↗
PubMed1984

The effects of dopaminergic blockade on serum TSH and prolactin levels in thyrotoxicosis.

In the first part of this study, we have demonstrated that, in 7 patients with untreated thyrotoxicosis, a 7 day regime of the long acting dopamine antagonist metoclopramide (10 mg orally 8 hourly) produces more adequate dopaminergic blockade at pituitary level than a single oral 10 mg dose of the compound as assessed by serum prolactin responses. Subsequently, we have employed this protracted oral metoclopramide regime to evaluate the contribution of dopaminergic tone to the abnormal TSH and prolactin responsiveness of thyrotoxicosis. Serum TSH and prolactin responses to iv TRH (200 micrograms) were measured in 10 untreated thyrotoxic patients before and after a 7 day period of metoclopramide 10 mg orally 8 hourly. Ten euthyroid individuals were studied in similar fashion, their serum samples being analysed for prolactin levels alone, thus providing a control group for prolactin responsiveness to TRH, before and after metoclopramide. In the thyrotoxic patients basal TSH levels did not change as a consequence of metoclopramide therapy and the TSH response to TRH remained flat. Basal prolactin levels were similar in thyrotoxic and euthyroid individuals and the increase in prolactin, seen in both groups after metoclopramide, was smaller in the thyrotoxic group than in the euthyroid group. Prolactin responsiveness to TRH was significantly impaired in the thyrotoxic subjects as compared to euthyroid subjects. After metoclopramide there was a significant decline in prolactin responsiveness in the euthyroid group, and a similar, though insignificant, trend in the thyrotoxic patients. We conclude that in thyrotoxicosis dopaminergic tone plays no major part in the suppression of TSH levels, nor in the impaired prolactin responsiveness to TRH.

Administration, Oral↗
PubMed2002

Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats.

OBJECTIVE: The present experiments were designed to investigate the influence of the renin--angiotensin system (RAS) on prolactin secretion in response to hemorrhage (1.2 ml/100 g body weight (bw)/2 min). METHODS AND RESULTS: Male Wistar rats (250-300 g) were divided into the following experimental groups. (i) Sham-operated animals submitted to intravenous administration of [Sar(1),Thr(8)]-angiotensin II (sarthran), an angiotensin II antagonist (750 ng/100 g bw as a bolus plus an infusion of 25 ng/100 g bw/min over 30 min), which did not alter the prolactin secretion in response to hemorrhage. (ii) Animals submitted to adrenodemedullation which by itself increased the prolactin secretion in response to hemorrhage by 274% (P<0.01). However, sarthran infusion into adrenodemedullated rats completely blocked this increased prolactin secretion in response to hemorrhage (P<0.01). (iii) Intact animals submitted to blockade of sympathetic noradrenergic pathways by pretreatment with guanethidine (10 mg/100 g bw), which also increased the prolactin secretion in response to hemorrhage by 55% (P<0.01). This increased prolactin secretion in response to hemorrhage observed in guanethidine-treated rats was completely blocked by sarthran preinfusion (P<0.01). (iv) Adrenodemedullated animals pretreated with guanethidine, which abolished the prolactin secretion induced by hemorrhage. CONCLUSIONS: Our data suggest a role for circulating catecholamines in the prolactin secretion response to stress. In addition, the experiments reported here demonstrate that RAS has a stimulatory effect on prolactin secretion in circumstances in which sympathetic activity or adrenomedullary secretion is suppressed. These are the first data demonstrating that a physiological prolactin secretion response to stress depends on the RAS.

Adrenal Medulla↗
PubMed1982

Prolactin response in beef cows and heifers suckling one or two calves.

Blood was collected, at 5-min intervals for 3 h, via jugular cannulation every 14 days during the first 4 months post partum from beef cows and heifers, 4 suckling 2 calves and 4 suckling 1 calf. Calves were isolated from the dams to prevent suckling for approximately 4 h before and 2 1/2 h during sampling to obtain baseline values for prolactin, measured by radioimmunoassay. During the last 30 min of sampling, calves were allowed to suck. Milk samples were also collected at 28-day intervals from 60 females, 30 with twins and 30 with single calves. beginning 2 weeks after calving and continuing until calves were weaned at 180 days of age. No differences were observed between dams with 1 and 2 calves for baseline plasma prolactin level or for prolactin response to the suckling stimulus by 1 or 2 calves. However, milk prolactin concentration was significantly higher (P less than 0.01) for dams with 2 calves, probably reflecting the more frequent suckling that occurs with twins. Milk prolactin value in this study was not highly correlated with the post-partum interval to first ovulation from another study on these animals. It is concluded that prolactin is not significantly higher (P less than 0.01) for dams with 2 calves, probably reflecting the more frequent suckling that occurs with twins. Milk prolactin value in this study was not highly correlated with the post-partum interval to first ovulation from another study on these animals. It is concluded that prolactin is not significantly higher (P less than 0.01) for dams with 2 calves, probably reflecting the more frequent suckling that occurs with twins. Milk prolactin value in this study was not highly correlated with the post-partum interval to first ovulation from another study on these animals. It is concluded that prolactin is not the primary factor controlling the longer post-partum interval to first ovulation in beef cattle with twins.

Animals↗
PubMed1986

Prolactin administration during the luteal and follicular phase of the oestrous cycle of gilts.

In Exp. I infusions of prolactin (0.5 mg in 2 ml sterile saline) were repeated every 2 h for 36 h on Days 12-13 of the cycle. In Exp. II infusions of prolactin were administered from Days 17 to 19 (60 h) at 2-h intervals. Control gilts were given 2 ml sterile saline at similar intervals during the same period. Basal prolactin concentrations before initiation of infusions ranged from 1.3 +/- 0.1 to 5.6 +/- 2.2 ng/ml in both experiments. By 5 min after a prolactin infusion, mean plasma prolactin concentration ranged from 74.9 +/- 5.8 to 113.0 +/- 9.5 ng/ml, but then declined to approximately equal to 10 ng/ml just before the next infusion of prolactin. Administration of prolactin during the luteal phase of the oestrous cycle of the gilts had no effect on basal levels of progesterone, oestradiol or LH. During the follicular phase there were no differences (P greater than 0.05) between control and prolactin-treated gilt progesterone and LH concentrations, but oestradiol plasma values were decreased (P less than 0.05) on the 2nd and 3rd day of prolactin treatment. Our results would indicate that prolactin does not play a major role in the regulation of the oestrous cycle of the pig.

Animals↗
PubMed1997

Prolactin-induced termination of obligate diapause of mink (Mustela vison) blastocysts in vitro and subsequent establishment of embryonic stem-like cells.

The mink reproductive cycle includes an obligatory period of embryonic diapause and delayed implantation, which continues in vitro and reduces the efficiency of embryonic stem (ES) cell establishment. Blastocysts recovered on day 7 and on days 13-16 after final mating were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with various concentrations of prolactin to determine optimal conditions for embryo attachment and subsequent establishment of embryonic stem cells. Five treatments were applied to both ages of blastocyst: A, DMEM control (n = 16); B, DMEM + 5 micrograms prolactin ml-1 after 10 days initial culture in DMEM alone (n = 17); after 1 day of initial culture: C, DMEM + 10 ng prolactin ml-1 (n = 17); D, DMEM + 1 microgram prolactin ml-1 (n = 19); and E, DMEM + 5 micrograms prolactin ml-1 (n = 17). Prolactin terminated diapause of day 13-16 blastocysts at all concentrations tested. The maximum attachment of embryos in vitro and subsequent production of ES-like cells occurred in medium supplemented with 5 micrograms prolactin ml-1. Prolactin did not affect attachment rates for day 7 blastocysts when 5 micrograms prolactin ml-1 was added, but prolactin at concentrations of 1 microgram ml-1 and 5 micrograms ml-1 when added on day 1 of culture enhanced ES-like cell line establishment. Two principal cell types were observed in the colonies: small stem cells and trophoblast-like cells with large areas of cytoplasm. The morphological evaluation of mink ES-like cell colonies was confirmed by cytochemical staining for alkaline phosphatase. Mink embryonic stem-like cells were found to stain positive for alkaline phosphatase. Alkaline phosphatase activity was lost upon cellular differentiation.

Alkaline Phosphatase↗
PubMed1992

Phosphorylation of prolactin and growth hormone.

To determine whether GH and prolactin could be phosphorylated, turkey GH, chicken GH, chicken prolactin and turkey prolactin were incubated in vitro with the catalytic subunit of protein kinase A and [gamma-32P]ATP. Phosphorylation was assessed after sodium dodecyl sulphate-polyacrylamide gel electrophoresis, Western blotting and autoradiography. Polyacrylamide electrophoresis showed that both purified native chicken GH and turkey GH were phosphorylated under the conditions employed. However, the glycosylated variant of chicken GH did not appear to be labelled. Chicken prolactin, turkey prolactin and the glycosylated variant of turkey prolactin were all intensely phosphorylated by protein kinase A. Ovine and rat prolactins could also be phosphorylated by protein kinase A. The phosphate content of different native prolactin (turkey, ovine and rat) and GH (ovine and chicken) preparations was also determined and found to be significant. Chicken pituitary cells in primary culture incorporated 32P in GH- and prolactin-like bands isolated by non-denaturing polyacrylamide gel electrophoresis, and this was stimulated by phorbol myristate acetate. Phosphorylation of GH and prolactin may thus explain some of the charge heterogeneity of these hormones.

Animals↗
PubMed2002

An Ets motif in the proximal decidual prolactin promoter is essential for basal gene expression.

Transcriptional regulation of the prolactin gene in the decidua differs from that in the pituitary. Several lines of evidence strongly suggest this difference is due to regulation of the prolactin gene in the decidua and other extra-pituitary tissues by tissue-specific transcription factors, which activate distinct promoters to induce prolactin gene expression in extra-pituitary sites compared with the pituitary. The human decidua is a major site of extra-pituitary expression of the prolactin gene. Here we present evidence that the transcription factor Ets-1 is critical for basal expression of the decidua-type (or decidual) prolactin promoter. Overexpression of Ets-1 significantly induces decidual prolactin promoter activity in BeWo and JAR cells that express little or no endogenous Ets-1. Conversely, a dominant/negative mutant of Ets represses basal promoter activity. Although the proximal 1.5 kb of the decidual prolactin promoter contains six Ets motifs, only the Ets motif at nt -77/-71 is essential for basal gene expression. Mutation of the Ets motif at nt -77/-71 results in an approximately 90% decrease in promoter activity, while mutation of the other Ets motifs results in only small changes. Electrophoretic mobility shift assays demonstrate that Ets proteins in decidualized endometrial stromal cells bind this Ets motif in the decidual prolactin promoter. Ets protein expression increases up to 20-fold upon induction of decidualization in endometrial stromal cells under conditions in which expression of the prolactin gene is also induced. These studies provide strong evidence for a critical role of the Ets transcription factor in basal expression of the decidual prolactin promoter.

Base Sequence↗
PubMed1977

Metabolic clearance of rat prolactin in the lactating and non-lactating rat.

The metabolic clearance of rat prolactin, assessed by the continuous infusion to equilibrium method, increased from 0-77 to 2-15 ml/min in lactating and from 0-65 to 1-75 ml/min in non-lactating rats as the infusion rate was increased from 100 to 472 ng/min. The clearance rate of rat prolactin did not increase when large doses of ovine prolactin were infused simultaneously with rat prolactin. The clearance rates computed from equilibrium levels of immunoreactive 131I-labelled rat prolactin in plasma were highly correlated with, but were considerably greater than, those computed from unlabelled rat prolactin which was infused simultaneously. In lactating and non-lactating rats, the clearance of each prolactin tested (RP-1, B-1, Nicoll's secreted and 131I-labelled) increased and had stabilized within the 30-35 min of infusion of each new higher dose of the hormone. The ability of the rat to clear quickly greater amounts of prolactin from the circulation as the infusion rate increases implies that plasma prolactin concentrations do not necessarily mirror the rate of prolactin secretion from the pituitary.

Animals↗
PubMed1977

Autoradiographic localization of the binding of 125I-labelled prolactin to rat tissues in vitro.

The binding of 125I-labelled prolactin to normal rat tissues was examined with autoradiographic techniques. Tissue slices were incubated with 125I-labelled ovine prolactin in the presence or absence of excess unlabelled hormone to distinguish between the specific and the non-specific localization of grains. Specific binding was found in the liver, adrenal gland and kidney from female rats, and in the mammary gland, ovary, testis and prostate gland. Conversely, fat, muscle, heart, lung, and spleen from female rats and uterine tissue did not bind 125I-labelled prolactin appreciably, or show competition for binding in the presence of unlabelled hormone. In the testis, prolactin bound exclusively to Leydig cells; in the prostate gland, binding was localized in the secretory epithelium. Kidney tubules in the cortex displayed specific prolactin localization whereas the medulla did not bind prolactin. Adrenal medulla showed no hormone binding; however, the zona reticularis and to a lesser extent the zona fasciculata bound prolactin. In the ovary, grains were limited to the theca and to a lesser extent the corpus luteum and follicles. In all cases, binding was essentially abolished when unlabelled prolactin was included in the incubation medium. These results confirm reports of the presence of prolactin receptors in these tissues and serve to identify the cells within a particular organ that respond to prolactin.

Adrenal Glands↗