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PubMed1995

Concentrations of prolactin and prostaglandins during and after cardiopulmonary resuscitation.

OBJECTIVES: To assess differences in plasma prolactin and prostaglandin concentrations in resuscitated and nonresuscitated patients during cardiopulmonary resuscitation (CPR), and to compare changes of prostaglandin and prolactin concentrations with hemodynamic variables in the immediate postresuscitation phase. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a university hospital. PATIENTS: Twenty-nine patients ranging in age from 39 to 87 yrs with out-of-hospital cardiac arrest. INTERVENTIONS: Venous blood samples were taken during CPR and at 5, 15, 30, and 60 mins after restoration of spontaneous circulation in order to measure plasma concentrations of prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 by immunoassay. Heart rate and blood pressure were measured at 5, 15, 30, and 60 mins after restoration of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: In 15 patients, restoration of spontaneous circulation was achieved; in the remaining 14 patients, successful resuscitation was not possible. During CPR, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 95.9 +/- 13.6 micrograms/L, 357 +/- 61 ng/L, 228 +/- 28 ng/L, 277 +/- 66 ng/L, and 375 +/- 78 ng/L, respectively, in resuscitated patients, and 23.9 +/- 5.6 micrograms/L (p = .0001), 192 +/- 22 ng/L (p = .005), 202 +/- 31 ng/L (p = .528), 221 +/- 40 ng/L (p = .713), and 344 +/- 77 ng/L (p = .780), respectively, in nonresuscitated patients. At 60 mins after restoration of spontaneous circulation, the mean plasma prolactin, prostaglandin F2 alpha, 15-keto-13,14-dihydro-prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2 concentrations were 50.1 +/- 9.5 micrograms/L, 306 +/- 42 ng/L, 503 +/- 87 ng/L, 278 +/- 55 ng/L, and 355 +/- 30 ng/L, respectively. Mean values of systolic arterial blood pressure were 114 +/- 12 mm Hg at 30 mins and 123 +/- 18 mm Hg at 60 mins. No significant correlations were found between hemodynamic values and plasma concentrations of prolactin or prostaglandins. CONCLUSIONS: Prolactin and prostaglandin concentrations were increased during cardiac arrest and CPR. Successful initial resuscitation was associated with increased prolactin and prostaglandin F2 alpha concentrations during CPR. Decreased concentrations in non-resuscitated patients may have been a result of exhaustion of the neuroendocrine and eicosanoid systems, or may be due to differences in bioavailability at the site of blood sampling based upon differences in hemodynamics.

Adult↗
PubMed1999

Prolactin levels and adverse events in patients treated with risperidone.

Hyperprolactinemia is a common clinical disorder that may lead to sexual dysfunction or galactorrhea. It may arise from a variety of etiologies, including the use of antipsychotic agents, presumably because of a dopamine receptor blockade. This analysis was designed to characterize the relationship between risperidone, serum prolactin levels, and possible clinical sequelae. All data from randomized, double-blind studies of risperidone in patients with chronic schizophrenia were analyzed. The two largest studies (the North American and multinational trials) included 841 patients (259 women, 582 men) with paired prolactin level data and 1,884 patients (554 women, 1,330 men) with data on six adverse events possibly associated with increased prolactin levels (amenorrhea, galactorrhea, and decreased libido in women; erectile dysfunction, ejaculatory dysfunction, gynecomastia, and decreased libido in men). Both risperidone and haloperidol produced dose-related increases in plasma prolactin levels in men and women. Among women, the risperidone dose was not correlated with adverse events, nor were the adverse events correlated with endpoint prolactin levels. Among men, the incidence of adverse events was positively correlated with risperidone dose; however, at risperidone doses of 4 to 10 mg/day the incidence of adverse events was not significantly higher than that observed in patients receiving placebo. Furthermore, adverse events in men were unrelated to plasma prolactin levels. Risperidone-associated increase in serum prolactin levels was not significantly correlated to the emergence of possible prolactin-related side effects.

Adult↗
PubMed2007

Prolactin release in children treated with risperidone: impact and role of CYP2D6 metabolism.

OBJECTIVE: Little is known about the role of CYP2D6 polymorphism in risperidone-induced prolactin release in children. METHOD: Twenty-five children (aged 5-15 years) with pervasive developmental disorders were genotyped for CYP2D6 polymorphisms. Serum prolactin, risperidone, and 9-hydroxyrisperidone were assessed at baseline and after 8 weeks of risperidone treatment (mean dosage, 0.06 +/- 0.03 mg/kg/d). After 24 weeks of treatment, prolactin was measured in a subsample of 15 children. Adverse effects were evaluated using a clinician-rated survey. RESULTS: Mean +/- SD prolactin levels increased from 7.8 +/- 8.0 ng/mL at baseline to 33.2 +/- 12.8 ng/mL at week 8 (P < 0.001), with a slight decrease to 28.8 +/- 13.6 ng/mL at week 24. At week 8, serum prolactin level was positively correlated with dose per kilogram (r = 0.648, P < 0.001), number of functional CYP2D6 genes (J = 2.117, P = 0.034), and serum 9-hydroxyrisperidone concentration (r = 0.664, P = 0.001) and was negatively correlated with the risperidone/9-hydroxyrisperidone ratio (r = -0.571, P = 0.004) but not with risperidone concentration (r = -0.243, P = 0.264) nor age (r = 0.072, P = 0.733). Prolactin elevation was not associated with adverse effects. CONCLUSIONS: Low-to-intermediate doses of risperidone induced a 4-fold prolactin increase in children without a clear development of tolerance up to 6 months. CYP2D6 ultrarapid metabolism may be a risk factor for more pronounced prolactin elevation.

Adolescent↗
PubMed1995

Influence of the dosing interval on prolactin release after remoxipride.

1. The prolactin response following administration of the D2-dopamine receptor antagonist remoxipride was studied in eight healthy male volunteers. The purpose of the study was to investigate the duration of a refractory period of prolactin release following two doses of remoxipride. A further aim was to compare the prolactin response following remoxipride and thyrotropin release hormone (TRH) during the refractory period. The subjects received two 30 min intravenous (i.v.) infusions of remoxipride 50 mg with different time intervals between the two doses, in a randomized six period crossover design. The time intervals between the two remoxipride doses were 2, 8, 12, 24 and 48 h. On one occasion the remoxipride dose was followed by an i.v. injection of TRH after 2 h. 2. The plasma peak prolactin concentrations obtained after the first remoxipride dose correspond to a maximal release of prolactin according to earlier studies. A small second peak of prolactin was observed after 2 h. The release was gradually increased with longer time intervals between the consecutive doses. The refractory period for a second prolactin release similar to the first one after remoxipride was found to be 24 h for most of the subjects. 3. TRH resulted in a faster and higher increase in prolactin response of a shorter duration than after remoxipride administered 2 h after the first dose.

Adult↗
PubMed1981

Serum prolactin levels in the prepubertal period in male and female rats. Control by photoperiod and gonadal status and relationship to puberty onset.

In female rats there is a temporary afternoon rise in prolactin during the transition from the weaning period to the period just preceding puberty. The purpose of this study was to determine whether a similar temporary prolactin peak occurs in males at the same age and to assess the dependence of this elevation upon gonadal status and light cycle cues. Blood samples were collected at 08.00, 20.00 h colony time during the prepubertal period. A prolactin peak occurred only at 28 days of age in males. This peak did not occur in either males or females gonadectomized at 22 days of age. Animals reared in constant light from weaning (21 days of age) failed to show an afternoon prolactin peak at 28 or 32 days of age. Animals in constant light from weaning age showed maximum prolactin at 08.00 h on days 28, 30, and 32 with minimum levels at 20.00 h. It can be concluded that both males and females exhibit a transient peak of prolactin during the prepubertal period. This peak was abolished by gonadectomy and by constant light, suggesting that it is an expression of a clock mechanism sensitive to photoperiod and gonadal steroids. The prolactin peak does not appear to correlate with pubertal onset per se since both vaginal opening and balanopreputial separation are precocious in constant light despite the fact that the prolactin peak is abolished in the population as a whole.

Aging↗
PubMed1984

Prolactin secretion in the human male is increased by endogenous oestrogens and decreased by exogenous/endogenous androgens.

There is evidence that prolactin may be involved in testicular steroidogenesis, and we have therefore investigated whether there is feedback regulation of androgens/oestrogens on prolactin secretion in the human male. To assess this we have measured basal and TRH-stimulated prolactin levels in: Six eugonadal men before and after 2 weeks' administration of the aromatase inhibitor delta'-testolactone, which led to a fall in oestradiol levels with unchanged levels of testosterone. In these patients, prolactin levels decreased. Six eugonadal subjects before and after 6 weeks' administration of dihydrotestosterone undecanoate. In these subjects, prolactin levels decreased. Six agonadal subjects, tested after 12 weeks' treatment with dihydrotestosterone undecanoate and compared to: Six agonadal subjects who received no sex steroid treatment. Again, it was found that dihydrotestosterone treatment decreased prolactin levels in patients from Group C. Six eugonadal subjects were also studied before and after 6 weeks' administration of the androgen receptor antagonist, spironolactone, and this treatment increased Prl secretion. It is concluded that in the human male, endogenous oestrogens increase prolactin secretion whilst exogenous/endogenous androgens decrease prolactin secretion.

Adult↗
PubMed1994

Photoperiodically-induced cycles in the secretion of prolactin in hypothalamo-pituitary disconnected rams: evidence for translation of the melatonin signal in the pituitary gland.

Long term changes in the secretion of prolactin were monitored in groups of hypothalamo-pituitary disconnected rams (HPD rams, n = 8) and control rams (HPD sham-operated and unoperated, n = 8) while exposed to an artificial lighting regimen of alternating 16-weekly periods of long days (16L:8D) and short days (8L:16D) for 72 weeks, and during a treatment with subcutaneous constant-release implants of melatonin under long days. The HPD rams showed all the clinical characteristics of complete pituitary disconnection (diabetes insipidus, gonadal regression and slight obesity), and were unresponsive to a range of provocation tests (exposure to a barking sheep dog, cannulation of the jugular vein, injection of serotonin and NMDA) which caused acute changes in the blood plasma concentrations of prolactin in the controls. Nevertheless, there was a clearly defined cycle in the blood concentrations of prolactin in the HPD rams related to the imposed lighting regimen with values 10-fold higher under long days compared to short days (HPD mean +/- SEM: 90.1 +/- 24.7 vs 9.4 +/- 2.0 micrograms/l, long vs short day respectively, P < 0.001). The temporal pattern was very similar to that observed in the controls, although the concentrations of prolactin were higher in the HPD rams and more variable (control mean +/- SEM: 55.6 +/- 3.6 vs 3.0 +/- 0.5 micrograms/l, long vs short day, P < 0.001). There was a corresponding cycle in the growth and moulting of the wool in the HPD rams consistent with a biological response to the photoperiodically-induced changes in the secretion of prolactin. The diurnal rhythm in the blood concentrations of prolactin was absent in the HPD rams, but there was a normal rhythm in the secretion of melatonin. The treatment of the animals with constant-release implants of melatonin under long days caused a marked decrease in the blood concentrations of prolactin in both the HPD and control rams. The overall conclusion is that the endogenously generated daily melatonin signal which encodes daylength acts directly in the pituitary gland to mediate the effects of photo-period on the secretion of prolactin. The photo-period transduction pathway thus by-passes the hypothalamus.

Aggression↗
PubMed2004

Inter-relationships between the secretory dynamics of thyrotrophin-releasing hormone, thyrotrophin and prolactin in periovulatory mares: effect of hypothyroidism.

We used our nonsurgical technique for collecting pituitary venous blood to relate the dynamics of thyrotrophin-releasing hormone (TRH) secretion to the secretion patterns of both prolactin and thyrotrophin in periovulatory mares, either euthyroid (n = 5) or made hypothyroid by treatment with propyl-thiouracil (n = 5). Pituitary venous blood was collected continuously and divided into 1-min aliquots for 4 h. To test the effect of dopamine on the relationship between secretion patterns, sulpiride, a selective D2 receptor antagonist, was given i.m. after 2 h of sampling. Thorough testing of the model and blood collection procedure revealed no sites of TRH loss. Hypothyroidism increased the mean secretion rates of TRH (P = 0.04) and thyrotrophin (P < 0.0001) but not prolactin. Sulpiride increased prolactin secretion rates in hypothyroid (P < 0.0001) and control (P = 0.007) mares, but did not alter TRH or thyrotrophin secretion rates. In both groups of mares, all three hormones were secreted episodically but not rhythmically. In both groups, the secretion pattern of TRH was almost always significantly related to that of thyrotrophin, as assessed by cross correlation and cross approximate entropy (ApEn) analysis. However, the degree of linear correlation was weak, with only 14% (hypothyroid) or 8% (controls) of the variation in thyrotrophin secretion rates attributable to TRH. Prolactin and TRH secretion patterns before sulpiride were coupled on cross ApEn analysis in both groups, and the minute-to-minute secretion rates of the two hormones were correlated in four hypothyroid and three euthyroid mares. Overall, the small, but significant, degree of association between TRH and prolactin was similar to that between TRH and thyrotrophin. In hypothyroid mares, sulpiride increased (P = 0.02) the synchrony between TRH and prolactin patterns. We conclude that in horses: (i) little TRH degradation occurs during passage through the pituitary or in blood after 1 h at 37 degrees C; (ii) TRH is not the major factor controlling minute-to-minute fluctuations in either thyrotrophin or prolactin; and (iii) reducing two strongly inhibitory inputs (i.e. dopamine and thyroid hormones) may magnify the stimulatory effect of TRH on prolactin secretion.

Animals↗
PubMed2005

Prolactin, a natriuretic hormone, interacting with the renal dopamine system.

BACKGROUND: Although prolactin affects sodium and water transport across the plasma membrane and interacts with dopamine in the brain, its role in the kidney is unclear. Here we examined the effect of prolactin and its possible interaction with the intrarenal natriuretic hormone dopamine, on proximal tubular Na(+), K(+)-ATPase activity in vitro and renal function in anesthetized rats. METHODS: Na(+), K(+)-ATPase activity was measured as ouabain-sensitive adenosine triphosphate (ATP) hydrolysis in microdissected proximal tubular segments. Renal function was studied during euvolemic conditions by conventional clearance techniques. RESULTS: Prolactin induced a dose-dependent inhibition of proximal tubular Na(+), K(+)-ATPase activity. A maximal inhibitory effect of 48% of control was observed at an in vitro prolactin concentration of 1 microg/mL. This effect was completely abolished by a dopamine D1 receptor antagonist. In tubules preincubated with inhibitors of aromatic amino acid decarboxylase (AADC), the rate-limiting enzyme in renal dopamine formation, prolactin had no effect on Na(+), K(+)-ATPase activity. In rats, prolactin infusion resulted in an increase in urinary sodium, potassium, and water excretion. These effects were also completely abolished by the D1 receptor antagonist. Prolactin had no significant effects on glomerular filtration rate (GFR) or mean arterial blood pressure. CONCLUSION: We conclude that prolactin is a natriuretic hormone which interacts with the renal dopamine system for its effects. The natriuretic response is associated with inhibition of proximal tubular Na(+), K(+)-ATPase activity.

Animals↗
PubMed1999

Kinetics of serum neuron-specific enolase and prolactin in patients after single epileptic seizures.

PURPOSE: To investigate and compare the temporal profile of serial levels of neuron-specific enolase (NSE) and prolactin in serum from patients after single epileptic seizures. METHODS: Measurement of NSE and prolactin by sensitive immunoassays in 21 patients with complex partial seizure (CPSs: n = 11) and secondarily generalized tonic-clonic seizures (SGTCSs; n = 10) during continuous video-EEG monitoring at four different time points (1, 3, 6, and 24 h after ictal event). Statistical analysis was performed by using a repeated-measures analysis of variance (ANOVA) model. RESULTS: Mean+/-SD values for NSE levels (ng/ml) were 12.5 +/-4.4 (1 h), 10.8+/-3.8 (3 h), 11.1+/-4.9 (6 h), and 8.2+/-1.9 (24 h). The corresponding prolactin levels (mU/L) were 1,311+/-1,034, 232+/-158, 237+/-175, and 251+/-98. There was a significant decrease of NSE and prolactin levels over time (p < 0.001). The pair-wise comparison of NSE levels showed significant differences between the time points 1 vs. 24 h (p < 0.001), 3 vs. 24 h (p = 0.007), and 6 vs. 24 h (p = 0.009). In contrast, serum prolactin levels showed a significant difference between 1 vs. 3 h (p < 0.001) only. Most of the NSE levels remained normal after CPSs and SGTCSs. At 1 h after the seizure, only 33% of the subjects had increased NSE, whereas abnormal prolactin levels occurred with a sensitivity of 80%. CONCLUSIONS: In contrast to prolactin, serum NSE is not a sensitive marker of individual seizures. Only some individuals showed an increase of NSE beyond the prolactin-sensitive time frame after a single seizure, and mean NSE levels were not significantly increased compared with those of normal controls.

Adult↗
PubMed2003

Differential effects of age and sex on the postnatal responsiveness of brown adipose tissue to prolactin administration in rats.

Previous studies have shown that prolactin administration to pregnant rats results in offspring with enhanced abundance of the brown adipose tissue-specific uncoupling protein (UCP) 1. The present study therefore aimed to determine whether a similar effect was observed after birth and if the sex of the animal further influenced the responsiveness of brown adipose tissue mitochondria to prolactin administration. Daily prolactin injections were therefore commenced at 15, 35 or 60 days of age and continued for 4 days. The abundance of UCP1 was unchanged with age in females but decreased between 15 and 35 days in males and was lower in males than females by 60 days of age. Cytochrome c abundance remained unchanged with postnatal age in both males and females and was consistently higher in males at each sampling age. Prolactin decreased the abundance of UCP1 and cytochrome c when administered to female rats at 35 and 60 days of age, but had no effect at 15 days. In contrast, prolactin had no effect on UCP1 in male rats at any age, but did stimulate the abundance of cytochrome c at 15 days of age. In conclusion, the administration of prolactin to postnatal rats over the period in which maturation of the hypothalamic-pituitary axis and brown adipose tissue function is occurring did not enhance UCP1 abundance. In females, prolactin actually caused a reduction in UCP1 suggesting that in rats it is only prior to birth that prolactin has a stimulatory role on brown adipose tissue development.

Adipose Tissue, Brown↗
PubMed2004

Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats.

The present study evaluated the effect of acute extracellular volume expansion (EVE) induced by intravenous injection of isotonic (0.15 m NaCl) or hypertonic saline (0.3 m NaCl) on prolactin, corticosterone, vasopressin, oxytocin and atrial natriuretic peptide (ANP) secretion. Male Wistar rats were treated with bromocriptine, sulpiride or dexamethasone. After isotonic and hypertonic EVE, the control group showed a significant increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increase in ANP and oxytocin levels in response to hypertonic EVE was more pronounced than to isotonic EVE. Bromocriptine and sulpiride treatments did not modify corticosterone, ANP and oxytocin responses to either isotonic or hypertonic EVE. The increases in prolactin and oxytocin, but not ANP, were blocked in dexamethasone pretreated rats. In conclusion, isotonic or hypertonic EVE induced an increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increases in ANP and oxytocin were independent of plasma concentrations of prolactin. The increases in prolactin and oxytocin were blocked by the inhibition of the hypothalamo-pituitary-adrenal (HPA) axis by dexamethasone. However, dexamethasone did not alter the increase in ANP secretion induced by isotonic or hypertonic EVE. Therefore, prolactin might participate in regulation of the hydroelectrolytic balance in mammals; however, in the present study, there was no evidence for direct interaction with ANPergic and oxytocinergic systems. In addition, the responses of prolactin and oxytocin induced by isotonic or hypertonic EVE are modulated by the HPA axis.

Animals↗
PubMed1970

Effects of cations on prolactin and growth hormone secretion by rat adenohypophyses in vitro.

1. Explants of rat adenohypophyses were incubated in medium 199, Earle's saline, or modified Earle's saline (K-Earle's) with different calcium, magnesium, sodium and potassium concentrations for 4-6 hr at 37 degrees C in 5% CO(2) in O(2).2. The amount of prolactin and growth hormone in explants and in medium was estimated by disk electrophoresis and densitometry.3. Low calcium inhibited prolactin secretion by 40-60%. Low magnesium and slightly increased (5x) magnesium (4.1 mM) did not influence prolactin secretion in either 1.8 mM or low calcium, but 10 and 20 mM magnesium inhibited secretion by 50 and 70%, respectively. Inhibition of prolactin secretion by high magnesium was reversible.4. Decreasing sodium by 80% had no effect on prolactin secretion, but low sodium inhibited the sustained, although not acute, secretion of this hormone.5. Low potassium did not affect the secretion of either prolactin or growth hormone. Increased potassium (32 or 54 mM) slightly stimulated prolactin secretion by adenohypophyses of males but had no effect on the secretion of this hormone by female glands.6. In 1.8 mM calcium, growth hormone secretion by pituitaries of males and females was markedly stimulated by increased potassium, but it was not appreciably affected by high potasium in low calcium. Increased potassium did not stimulate growth hormone secretion in medium containing low sodium with normal calcium.7. Secretion of prolactin and growth hormone by rat adenohypophyses is dependent upon calcium, but only growth hormone secretion is markedly stimulated by increased potassium. The difference in responsiveness to increased potassium, between the somatotrophs and lactotrophs, may be related to the predominant mode of hypothalamic control of these hormones.

Animals↗
PubMed2002

The differential effects of atypical antipsychotics on prolactin elevation are explained by their differential blood-brain disposition: a pharmacological analysis in rats.

All atypical antipsychotics avoid extrapyramidal side-effects yet differ in their propensity to cause other side-effects, like prolactin elevation. We proposed that the atypical antipsychotics with a propensity for prolactin elevation would show a higher pituitary versus striatal D2 receptor occupancy. To investigate this hypothesis, we tested four atypical antipsychotics, two that are commonly associated with prolactin elevation (amisulpride and risperidone) and two that are less frequently associated (quetiapine and olanzapine). In particular, we calculated their ED(50) values to increase plasma prolactin and block peripheral pituitary D2 receptors to their ED(50) values to antagonize apomorphine-induced stereotypy and occupy central striatal D2 receptors. All antipsychotics dose dependently increased prolactin levels and antagonized apomorphine-induced stereotypy. However, the central to peripheral potency (ED(50) for apomorphine antagonism to ED(50) for prolactin elevation) differed remarkably across these drugs: amisulpride (21764), risperidone (14), quetiapine (10), and olanzapine (1.7). Compounds displaying a higher peripheral potency brought about higher prolactin levels for a given level of functional central antagonism. This dissociation between central and peripheral effects was explained by the differential occupancy of D2 receptors in the striatum versus in the pituitary [ratio of striatal/pituitary ED(50) values (milligram per kilogram) for D2 occupancy): amisulpride (17/0.026 = 654), risperidone (0.89/0.081 = 14), quetiapine (24/4.1 = 6), olanzapine (0.30/0.43 = 0.7). These results indicate that dissociation between central and peripheral D2 receptor occupancy is a major determinant of the degree of prolactin elevation observed at therapeutic doses.

Animals↗
PubMed1985

Detection of two chromatin proteins which bind specifically to the 5'-flanking region of the rat prolactin gene.

We employed a protein gel blotting procedure to search for nuclear proteins from rat pituitary cells that bind preferentially to the 5'-flanking region of the rat prolactin gene. By gel blots of chromatin proteins from GH3 rat pituitary tumor cells with a 32P-labeled prolactin genomic clone, we detected two major binding proteins with molecular weights of approximately 44,000 and 48,000, designated NP44 and NP48, respectively. Both NP44 and NP48 are minor chromatin proteins which are extracted at low salt concentrations (0.4 M NaCl) and exhibit a range of slightly acidic isoelectric variants. NP44 and NP48 were detected at similar levels in chromatin extracts of GH3 cells, the prolactin-negative GC cell variant of the GH3 cells, and normal rat pituitary tissue. Considerably lower levels of these two proteins were found in chromatin extracts from rat liver and rat C6 glial cells. NP44 and NP48 exhibit DNA sequence specificity, as evidenced by their strong binding to the upstream flanking region of the prolactin gene, but only very weak binding to plasmid DNA, rat prolactin or growth hormone cDNAs, or upstream flanking regions of two other rat genes. By analyzing subclones of a rat prolactin genomic clone, we established that NP44 and NP48 bind to at least two sites, which are located between 0.4 and 2.0 kilobases (region I) and between 2.0 and 4.8 kilobases (region II) upstream of the transcription initiation site. These findings are discussed in the context of a possible functional association between the strong binding of NP44 and NP48 to the prolactin 5'-flanking region and pituitary-specific expression of the prolactin gene.

Animals↗
PubMed1999

Postmortem prolactin as a marker of antemortem stress.

AIM: To determine whether raised prolactin concentrations could be identified using postmortem venous blood and whether the level of prolactin correlated with antemortem stress. METHODS: Blood was obtained from the right femoral vein of 100 random adult necropsy cases, all of whom had been dead less than four days. Prolactin was determined in the samples by microparticle immunoassay. The levels of prolactin obtained were then analysed in relation to sex and cause of death, with particular emphasis on a history of antemortem stress and drug use. RESULTS: Prolactin in all cases of trauma was in the normal range (up to 500 mU/l). In cases of sudden unexpected deaths the mean concentration was 533 mU/l (95% confidence interval (CI), 372 to 694 mU/l). Postoperative deaths or cases with chronic disease had a mean value of 1027 mU/l (95% CI, 735 to 1319 mU/l). Cases of suicide had a mean value of 1398 mU/l. Analysis of the suicides by sex showed a significant difference, the mean in female cases being 2072 mU/l compared with 692 mU/l in male cases. In three of the four female suicides with the highest prolactin, the hyperprolactinaemia might have been attributable to a drug effect, but one case still had unexplained hyperprolactinaemia. CONCLUSIONS: It is possible to detect prolactin reliably in postmortem venous blood samples. Prolactin values at necropsy differ according to the cause of death, with markedly higher values in postoperative deaths and in the chronically ill. Hyperprolactinaemia in cases of suicide is likely to result from the effects of the drugs used, but the levels were higher than previously reported.

Adult↗
PubMed1984

Interaction of prolactin (PRL) binding sites with PRL receptor antibodies in rat liver cells in suspension culture: effect of inhibitors of cellular functions.

We have recently demonstrated that prolactin is able to maintain the level of in receptors in cultured rat hepatocytes. This effect could be modulated by various inhibitors of cellular functions. We report here that an antibody developed against a partially purified prolactin receptor preparation can mimic this effect of the hormone (although to a lesser extent) and that drugs can modulate it in a similar manner. In particular, cycloheximide (50 micrograms/mL), which reduced basal receptor levels by approximately 40%, totally reversed the maintenance induced by the antireceptor serum. Actinomycin D (10 micrograms/mL), another protein synthesis inhibitor (at the transcriptional level), had no effect of basal receptor concentration, but counteracted by about one-half the antiserum-induced maintenance. This effect of actinomycin D is much clearer here than the effect previously observed on prolactin-induced receptor levels in rat liver cells in culture. The effect of dinitrophenol (1 mM) on basal levels was of limited amplitude but maintenance was again partly reversed by this drug. In accordance with previous results obtained with prolactin, chloroquine (100 microM) and colchicine (1 microM) failed to alter prolactin binding either in the absence or presence of 5% antireceptor serum. The effect of the antiserum indicates that prolactin itself is not required beyond the membrane for its effect on receptor regulation to be attained. These results also confirm our previous results with prolactin maintenance of prolactin receptor levels in rat liver cells in culture, that the mechanism of receptor maintenance appears to be due in part to a stimulation of receptor synthesis but to be independent of the internalization or of lysosomal degradation.

Animals↗
PubMed1982

A possible mechanism of inotropic action of prolactin on rat heart.

Prolactin possesses positive inotropic actions in isolated heart preparations although the mechanism of this influence is not understood. Our study was designed to investigate the mechanism of this effect on the rat heart. Prolactin (50 ng/ml) produced a time-dependent increase (60%) in contractile force that reached maximum after 30 min and remained steady for a further 30 min. A similar time-dependent phenomenon was seen with 200 ng/ml prolactin although the maximum inotropic effect was reduced. Indomethacin (30 micrograms/ml) significantly reduced the inotropic effect of both prolactin concentrations although the effect of the hormone was not related to the release of 6-keto-PGF1 alpha, the prostacyclin metabolite. Propranolol (1-20 micrograms/ml) significantly reduced the positive inotropic effect of prolactin. Prolactin however had no influence on myocardial adenylate cyclase activity. Hearts that were removed from animals pretreated with 1.25 or 2.50 mg/kg reserpine did not respond to prolactin administration. It is suggested that the inotropic influence of prolactin is mediated by endogenous catecholamine liberation.

6-Ketoprostaglandin F1 alpha↗