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PubMed1985

Plasma prolactin levels in patients with essential hypertension, malignant hypertension and secondary hypertension.

Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. From these results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences may partly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanism of plasma prolactin increment.

Adolescent↗
PubMed1990

Oxytocin and prolactin levels in breast-feeding women. Correlation with milk yield and duration of breast-feeding.

The aim of the present study was to examine suckling-related plasma levels of oxytocin and prolactin in early and established lactation and to correlate hormone profiles to success of lactation performance. Fifty-five primiparous women participated in the study. From each, 18 blood samples were drawn in connection with breast-feeding on day 4 post partum and after 3-4 months. Oxytocin and prolactin levels were determined with radio-immunoassay. Basal levels of both hormones were significantly higher 4 days post partum than 3-4 months later and after weaning. Basal prolactin levels fell significantly within 24 h of weaning. Oxytocin and prolactin levels rose in response to breast-feeding--an effect which persisted during the lactation period. The suckling-induced release of prolactin--but not that of oxytocin--was related to basal hormone levels. Basal as well as stimulated oxytocin levels obtained 4 days and 3-4 months post partum correlated significantly, indicating that each woman has an individual, characteristic level of this hormone. Milk yield did not correlate with oxytocin or prolactin levels, but prolactin levels recorded 3-4 months post partum did correlate with the remaining period of breast-feeding. In addition, mothers who breast-fed exclusively 3-4 months post partum had significantly higher oxytocin and prolactin levels than those who gave supplementary feed. There was a significant correlation between oxytocin levels at 4 days and birth weight of the infant.

Adult↗
PubMed1994

Temporal synergism of corticosterone and prolactin in the Syrian hamster, Mesocricetus auratus.

To augment the limited work reported in the literature regarding testing of the hormonal temporal synergism hypothesis in Syrian hamsters (Joseph MM, Meier AH. Proc Soc Exp Biol Med. 1974;146:1150-5), a large experiment with female hamsters was conducted. Forty-eight received corticosterone at 18:00 h on January 21, 23, 25, 27, and 29 and ovine prolactin at one of six times of day beginning January 22 for 8 days; 36 received saline (at 18:00) and prolactin at one of the six times of day for 8 days; 35 received only prolactin at one of the six times of day for 8 days; and 16 received no injections. Twelve hamsters receiving corticosterone and prolactin and eight uninjected hamsters were on running wheels. The corticosterone and prolactin group not on wheels had a body weight gain and no circadian rhythm of weight gain, but did have circadian rhythms of response in organ weight, per 100 g of body weight, and in weights of fat pads and uteri. The corticosterone and prolactin group with access to running wheels gained in body weight and had larger ovaries and smaller fat pads. Hamsters receiving saline and prolactin had a body weight gain, but had no circadian rhythms of response in organ weights. The hamsters receiving only prolactin gained in body weight but had no rhythms of response, except for unexpected circadian rhythms in body weight gain and weights of fat pads. The uninjected hamsters had a modest weight gain. Most or all hamsters with access to running wheels free-ran, and the corticosterone injections did not appear to synchronize the locomotor activity rhythms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1995

Partial uncoupling of luteinizing hormone and prolactin pulse coincidence in hyperandrogenemic women.

A partly synchronized pulsatile secretion of luteinizing hormone (LH) and prolactin has previously been suggested as an indication of the coupling of the respective pulse generators under certain conditions. In women with hyperandrogenemic chronic anovulation, episodic LH secretion is disturbed. It was, therefore, the aim of the present study to evaluate possible changes in episodic prolactin secretion pattern and in LH/prolactin co-pulsatility, and to relate the results to the accelerated LH pulse frequencies often seen in patients with hyperandrogenemic chronic anovulation. Blood samples of 32 patients with hyperandrogenemia were taken at 10-min intervals between 10.00 and 20.00. Nine regularly cycling women with normal hormone levels served as controls. In the women with hyperandrogenemia, despite an average 41% rise of LH pulse frequency, prolactin pulse frequency decreased slightly by 14% as compared to controls; no correlation between the two parameters was found (r = 0.162). The number of coincident LH and prolactin pulses increased continuously with accelerating LH frequency. The best fitting function was a hyperbola which was limited by the maximal observed prolactin frequency. As a consequence, the fraction of LH pulses that were co-secreted with prolactin episodes decreased with higher LH pulse frequencies, while the fraction of prolactin pulses concomitant with LH pulses increased. Our data provide evidence that in women with hyperandrogenemic chronic anovulation a pathological LH pulse frequency is no longer coupled with pulsatile prolactin secretion, suggesting an isolated alteration of the central neuronal control mechanism for LH secretion.

Adolescent↗
PubMed1996

Nasal spray administration of bromocriptine: pharmacology and effect on serum prolactin level in puerperal women.

This study was aimed at investigating the absorption of nasally administered bromocriptine and its effect on serum prolactin level. Fifteen physiologically hyperprolactinemia women who had asked to discontinue breast feeding received a single nasal spray administration of 0.8 mg bromocriptine. Serum prolactin levels were measured by radioimmunoassay at 30 and 15 min before drug administration, at the time of administration and at 15, 30, 60, 120, 240, 480 and 720 min after administration; bromocriptine was radioimmunoassayed in only five of the patients from time 0 to 720 min after administration. Serum bromocriptine levels increased rapidly after administration, reached a maximum at 120 min and thereafter declined slowly over the subsequent 10 h. As the bromocriptine level increased there was a decline in the serum prolactin level. The first significant decline in serum prolactin level compared with the baseline level occurred at 30 min after administration and the level continued to decrease significantly until time 120 min. Four hours after administration the mean serum prolactin level was within the normal assay range. The maximum decline in serum prolactin level was reached at 720 min after administration. Correlation analysis between serum bromocriptine and prolactin concentrations yielded a significant negative value between times 0 and 120 min after administration. There was no significant change in mean orthostatic systolic or diastolic blood pressure or in mean heart rate. Only one patient complained of headache and dizziness; another experienced mild transient nausea, and none had vomiting. Ten patients (66.67%) reported light endonasal burning and an unpleasant taste which subsided after a few minutes; no patient showed nasal irritation at nasal examination. In conclusion, nasal administration of 0.8 mg bromocriptine was effective in reducing the serum prolactin level for more than 12 h after administration without inducing significant side-effects.

Administration, Intranasal↗
PubMed1979

Variables associated with peripartum traits in dairy cows. IV. Seasonal relationships among temperature, photoperiod, and blood plasma prolactin.

Concentrations of prolactin in plasma were measured in 176 dairy cows and heifers from 13 days before calving to 2.5 days after calving over 21 mo. Prolactin averaged 35.1, 115.0, and 34.4 ng/ml prepartum (days -13 to -2), peripartum (days -1.0 to +.5), and postpartum (days +1.5 and +2.5). Season of the year affected prolactin in all periods. The linear covariate of daily photoperiod (hours of daylight per 24 h) accounted for as much variation in prolactin prepartum and postpartum as did linear covariates of both photoperiod and average daily temperature. However, it was possible to account for additional seasonal variation in prolactin peripartum by addition of the temperature covariate to the photoperiod covariate. Although photoperiod was related either directly or indirectly more than temperature to factors affecting prolactin seasonally, these statistical inferences cannot prove that prolactin is more dependent on photoperiod than on temperature because the two metereorological measures were correlated (r = .84). When the data were grouped for correlation analysis by months, correlations between temperature and prolactin among prepartum samples collected in the spring and in the fall were positive, small but significant.

Animals↗
PubMed1984

Effect of presence of calf on milking-induced release of prolactin and oxytocin during early lactation of dairy cows.

The ability of dairy cows to release either prolactin or oxytocin in response to machine milking in a conventional milking parlor was reduced among cows maintained with their calves during the 1st wk postpartum. However, presence of the calf caused no prolonged inhibition; cows evaluated 9 or 23 days after calf removal released similar quantities of prolactin and oxytocin after milking compared to controls (cows whose calves were removed within 24 h after parturition) at the same stage of lactation. Ambient temperature on the day of sampling was positively associated with the premilking serum prolactin concentration among cows housed with or without their calves (correlation coefficients were .52 and .59), but neither ambient temperature nor premilking serum prolactin concentrations were closely associated with area under milking-induced prolactin response curves (correlation coefficients from -.15 to .18). Unlike basal serum prolactin concentration, ambient temperature on the day of sampling was not closely associated with premilking serum concentrations of oxytocin or quantities released to the milking stimulus (correlation coefficients from -.19 to -.12). These results confirm that the calf can inhibit maternal secretion of prolactin and oxytocin in the dairy cow. These data also indicate that the capacity of the cow to respond to the milking stimulus is independent of premilking serum concentrations of prolactin or oxytocin. Better understanding of factors that regulate the secretion of these hormones at milking may allow development of techniques to enhance hormonal response to milking stimuli and possibly enhance milk production.

Animals↗
PubMed1986

Variation among species in the endocrine control of mammary growth and function: the roles of prolactin, growth hormone, and placental lactogen.

Prolactin, growth hormone, and placental lactogen form a family of structurally related hormones, which may have evolved from a common ancestral peptide. Prolactin and growth hormone are present in all mammals, but the biological activity associated with placental lactogen has been detected in only some groups. Attempts to detect placental lactogen using bioassay and radioreceptor assay are reported and have been unsuccessful in an insectivore (the shrew), a bat, an edentate (the armadillo), a lagomorph (the rabbit), several carnivores (dog, cat, ferret), perissodactyls (horse, zebra, rhino), and, within the artiodactyls, pigs. Placental lactogenic activity has been detected in primates (chimpanzee, orangutan), rodents (voles, Pinon mouse, guinea-pig, mara), and in numerous artiodactyls (llama, giraffe, several species of deer, antelope, gnu, gazelle, musk ox, cape buffalo, Barbary sheep, several sheep of the genus Ovis, goat, and cow). These results confirm and extend the work of others and are discussed in relation to the evolution of these hormones. In synergism with steroid and thyroid hormones, protein hormones of the prolactin and growth hormone family play a crucial role in stimulating the development of the mammary gland, the differentiation and function of mammary cells to secrete milk, and in the systemic adjustments in maternal metabolism in pregnancy and lactation. Studies in vitro have shown that mammary tissues from several species synthesize milk components in response to insulin plus adrenal corticoid plus prolactin. However, there are also species differences in minimal hormonal requirements for lactogenesis. In vivo, for example, rabbits will initiate or sustain lactation in response to prolactin alone, whereas sheep and goats require prolactin plus growth hormone plus adrenal corticoid plus thyroid hormone. Measurement of hormone concentrations in the plasma of pregnant animals shows considerable differences among species in the pattern of secretion of lactogenic hormones to bring about mammary development. A surge of prolactin secretion occurs at parturition but may not be essential in the initiation of lactation. The timing of progesterone withdrawal correlates well with lactogenesis in eutherian mammals, but species differ in the mechanisms at parturition which bring this about. Marsupials show a quite different pattern of suckling-induced lactation. In maintaining lactation the greatest contrast is between ruminants, in which growth hormone is of particular importance, and other mammals, in which reduction of prolactin secretion with bromocriptine rapidly suppresses milk synthesis and secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Inhibition of prolactin secretion delays extinction of circadian LH surges in ovariectomized rats bearing estradiol implants.

Ovariectomized rats bearing Silastic capsules containing estradiol exhibit a daily afternoon surge of luteinizing hormone (LH) which decreases with time until it is undetectable by Day 10 after implantation of estradiol. Increases in basal prolactin levels as well as afternoon surges are also observed. To determine if increased prolactin secretion contributed to the extinction of the circadian LH surges, we examined the patterns of LH and prolactin secretion in rats in which prolactin was suppressed by bromocriptine treatment. In vehicle-treated control rats, the magnitude of the LH surges decreased with time. Large LH surges were observed on Days 2 and 4. A significant decrease in the surge occurred on Day 6, and it disappeared by Day 10. Animals treated with bromocriptine also exhibited large LH surges on Days 2 and 4, and in addition, secreted a greater amount of LH than the control group on Days 6, 8, and 10. In ovariectomized rats bearing estradiol implants, large afternoon surges in prolactin were observed and by Day 6, basal prolactin levels were also elevated. Bromocriptine treatment completely suppressed prolactin secretion through Day 6, but a small afternoon rise was observed on Days 8 and 10. These findings suggest that elevated prolactin secretion may be one factor contributing to the extinction of circadian LH surges in the estrogen-treated rat.

Animals↗
PubMed1989

Prolactin sensitivity of mammary epithelial cells from mice exposed neonatally to diethylstilbestrol.

We examined the responsiveness to prolactin and growth hormone of mammary epithelial cells from mice exposed neonatally to diethylstilbestrol (DES) and from control mice. The mammary epithelial cells were cultured inside collagen gels with serum-free medium containing insulin, epidermal growth factor, and linoleic acid. This produces prolactin-sensitive cells with low levels of casein production, as measured in cellular homogenates with a specific enzyme-linked immunosorbent assay for alpha-casein. The collagen gels containing these cells were then released and the medium supplements changed to insulin, linoleic acid, and prolactin at concentrations from 10 to 1000 ng/ml and growth hormone at 0, 10, or 100 ng/ml. This second phase of the culture, the differentiation phase, allows the cells to accumulate casein if they have this capacity. When cultured with prolactin only (no growth hormone), the cells from DES-exposed mice consistently accumulated 50-100% of the casein content of normal cells, but never more. Growth hormone, when added to prolactin-containing medium, increased casein accumulation above the levels seen with prolactin alone. Combinations of prolactin and growth hormone enhanced the difference between casein accumulation in DES-exposed and control cells, and DES-exposed cells were much less responsive to growth hormone. In our studies, the isolated mammary epithelial cells of estrogen-exposed mice are not more sensitive to prolactin than cells from normal animals as previous reports reports had suggested, but rather are generally less sensitive to hormonal stimulants.

Animals↗
PubMed1992

Temporal effects of estradiol and diethylstilbestrol on pituitary and plasma prolactin levels in ovariectomized Fischer 344 and Holtzman rats: a comparison of radioimmunoassay and Nb2 lymphoma cell bioassay.

An Nb2 lymphoma cell bioassay (Nb2BA) and a radioimmunoassay (RIA) were used to compare plasma and pituitary levels of prolactin in ovariectomized Fischer 344 (F344) and Holtzman rats treated with either diethylstilbestrol (DES) or estradiol for up to 8 weeks. The objectives were to determine whether there were temporal differences in prolactin responses in strains with different genetic predispositions to estrogen-induced pituitary tumor formation and to determine whether the results of the two assay methods were equivalent. All rats were ovariectomized for 7 days and all except controls received subcutaneous Silastic implants of DES or 17 beta-estradiol and were sacrificed at intervals from 2 days to 8 weeks later. Pituitary content and plasma levels of prolactin were determined by Nb2BA and RIA and the ratio of these measurements was calculated. DES induced a significant increase in pituitary prolactin in F344 rats by 2 days of treatment, as measured by RIA. Pituitary content increased to a peak by Day 4, after which a gradual decline occurred until the end of the experiment. Nb2BA measurements were similar to those obtained by RIA, except at 8 weeks, when the content determined by Nb2BA was significantly higher than the content determined by RIA. When estradiol was given to F344 rats a pattern of increase and subsequent decrease in pituitary content similar to that seen with DES was observed and levels measured by Nb2BA and RIA were essentially equivalent. Plasma levels of prolactin in DES-treated F344 rats increased exponentially through the 8 weeks, and the Nb2BA measurements were significantly greater than levels determined by RIA throughout the treatment period. Estradiol treatment produced a pattern of change in plasma levels of prolactin similar to that observed with DES, except that RIA and Nb2BA measurements were not different. Comparable results were obtained in Holtzman rats, except plasma levels were not increased to the same degree as seen in F344 rats. From these results, we conclude that DES, but not estradiol, can selectively increase the secretion of prolactin that is more bioactive than immunoreactive and that this effect of DES is observed in F344 and Holtzman rats, although F344 rats released more prolactin in response to estrogens than did Holtzman females.

Animals↗
PubMed1997

Effects of epidermal growth factor (EGF) and prolactin on EGF receptor cytoskeletal association in mammary epithelial cells.

Prolactin treatment of NMuMG mammary epithelial cells inhibits the ability of epidermal growth factor (EGF) to transduce a variety of signals, possibly by interfering with receptor tyrosine phosphorylation. However, the mechanism by which prolactin inhibits EGF receptor signaling is unclear. The objective of this study was to evaluate the effects of prolactin on the dynamics of EGF receptor degradation and resynthesis, and on the association of the receptor with the cytoskeleton. EGF decreased the EGF receptor content of NMuMG cells, and this decrease was unaffected by prolactin treatment. Subsequent to the decrease in EGF receptors, cells reaccumulated EGF receptors, and this re-accumulation was also unaffected by prolactin. In other studies, EGF induced a rapid association of EGF receptor with Triton X-100-insoluble (cytoskeletal) elements. The cytoskeletally associated receptors were more heavily tyrosine phosphorylated than soluble receptors in the absence of prolactin. In the presence of prolactin, similar amounts of EGF receptor associated with the cytoskeleton, but both cytoskeletal and soluble receptors exhibited decreased tyrosine phosphorylation. These studies indicate that the effects of prolactin on EGF receptor signaling are not likely to be due to altered receptor dynamics or cytoskeletal association but are more likely due to an alteration in receptor kinase activity.

Animals↗
PubMed1976

Growth hormone and prolactin in the fetus.

Growth hormone is released from pituitary glands maintained in tissue culture as early as 5 weeks after conception. It has been identified in the fetal anterior pituitary gland by immunologic and biologic techniques between 7 and 15 weeks of gestation. Immunoreactive pituitary GH levels increase rapidly between 10 and 14 weeks of gestation to maximal levels at 30-34 weeks. Serum GH levels are detectable by 10-weeks postconception and reach maximal values at 20-24 weeks declining thereafter until term. Pospartum GH concentrations decline over several weeks to lower values, GH levels remaining higher in preterm than in term infants. The biologic role of pituitary GH in the fetus is unknown. Although birth-weights and lengths are reported to be normal in infants with anencephaly, aplasia, or hypoplasia of the pituitary gland and in isolated deficiency of growth hormone, in whom pituitary and serum GH levels are low, careful inspection of large series of such infants reveals that their birthweights may indeed be low and that cell numbers in many organs may be subnormal. In experimental animals prenatal administration of GH increases maternal weight and gestational length. Reported effects on neuronal growth and adult intelligence of animals treated prenatally may reflect these phenomena rather than a direct transplacental effect of GH. Prolactin is also elaborated by the pituitary gland of very young human fetuses. It has been identified immunologically by 10-weeks gestation and biologically at 18 weeks. Pituitary content of immunoreactive prolactin remains low until 16.5-weeks gestation and then increases steadily until term. The plasma concentration of prolactin is low until 30-weeks gestation and increases thereafter until term. In anencephalic fetuses prolactin levels are normal and respond to appropriate stimuli. Very high concentrations of (possibly fetal) prolactin are found in the amniotic fluid. The role of prolactin in the fetus is also unknown. It has been suggested that prolactin may be important for growth of the fetal adrenal cortex and/or for suppression of the immune response during pregnancy. It is apparent that a great deal of additional work is necessary before the importance of either growth hormone of prolactin for normal fetal growth and development will be known.

Animals↗
PubMedDate not supplied

[Effect of prolactin in different culture systems on maturation of bovine oocytes and their ability for further development].

We studied the influence of bovine prolactin on the maturation of cumulus-enclosed bovine oocytes in different culture systems as well as on their capacity for subsequent development after in vitro fertilization. The prolactin effect on chromosome transformations in oocytes depended on the hormone concentration in the medium with fetal calf serum. Prolactin at 50 ng/ml proved to stimulate nuclear maturation of the oocytes. This concentration was used to compare various systems of oocytes cultivation. The prolactin effect on bovine oocytes maturation and their capacity for subsequent development depended on the composition of the cultivation medium. The introduction of prolactin into the medium with fetal calf serum, estradiol, and follicle-stimulating hormone had no effect on the reinitiation of meiosis in the oocytes but stimulated its completion, which increased the proportion of the oocytes at the telophase I and metaphase II stages as well as the proportion of the eggs cleft after fertilization. Prolactin affected neither the nuclear maturation nor the capacity for further development of the oocytes cultivated in the medium with serum of estrous cows. The addition of prolactin to the medium with calf serum where the oocytes and granulosa cells were cocultured increased the subsequent yield of the embryos developed to the morula and blastocyst stages. In this culture system, the hormone did not affect the rate of oocytes that reached the final stages of meiosis but inhibited their transition from telophase I to metaphase II. We propose that prolactin may favor the completion of cytoplasmic modifications going into the maturing oocyte.

Animals↗
PubMed1979

Comparison of the effects of deafferentation and ablation of medial basal hypothalamus on thyrotropin and prolactin secretion.

To further delineate the interrelationships of neural control of TSH and prolactin secretion, medial basal hypothalamic deafferentation (MBHD) or medial basal hypothalamic ablation (MBHA) were performed in euthyroid or hypothyroid male rats. MBHD produced a prompt and significant fall in plasma TSH but no change in plasma prolactin. MBHA produced a more marked fall in plasma TSH and a 6-fold rise in plasma prolactin within 3 days postoperatively. Plasma TSH remained at a low level postoperatively, but plasma prolactin gradually declined from its peak 3-5 days postoperatively to approximately the initial basal levels 2 weeks postoperatively. MBHA did not appreciably impair the ability of TRH to stimulate TSH secretion or of perphenazine to stimulate prolactin secretion. Where the same experiments were performed in both euthyroid and hypothyroid rats, there was no qualitative difference between the two, although basal plasma TSH was higher and prolactin lower in the hypothyroid than in the euthyroid animals. Our data support the concept that the medial basal hypothalamus is important in stimulating TSH and inhibiting prolactin secretion. Dormant inhibitory influences on prolactin secretion, but not stimulatory influences on TSH secretion, may be aroused after hypothalamic ablation.

Animals↗
PubMed1992

The retino-hypothalamic tract is involved in prolactin regulation in fetal sheep.

To investigate the role of the retino-hypothalamic tract on fetal prolactin regulation, we examined the effect of ocular enucleation on fetal plasma prolactin. Eleven fetuses of Suffolk ewes were chronically catheterized during fall, and six of them were subjected to bilateral ocular enucleation. All ewes were kept at 12h:12h light:dark cycle (lights on at 0800 and off at 2000). The experiments were performed 5-9 days after surgery (GA control fetuses 125 +/- 1.5, optical enucleation 121.3 +/- 1.5 days). Blood samples were taken from fetuses hourly around the clock, and plasma prolactin and cortisol were measured by radioimmunoassay (RIA). Luteinizing hormone (LH) and Growth hormone (GH) were measured in pooled plasma samples from control and enucleated fetuses by RIA. Average plasma prolactin was 5-fold lower in enucleated than in control fetuses (9.6 +/- 0.5 and 54.2 +/- 3.3 ng/ml, SEM; P < 0.005). Both control and enucleated fetuses presented circadian rhythm of prolactin with acrophase between 1400 and 1830 h. An enucleated fetus was tested for response of prolactin to TRH. Prolactin increased as described in the literature. There was no change in plasma concentration of cortisol, LH or GH after ocular enucleation. Our data indicate that the optical pathway participates in prolactin regulation in the fetal sheep.

Animals↗
PubMed1992

Binding and growth-stimulation of cervical cancer cell lines by prolactin.

Two cervical cancer cell lines CC7-T and Si-Ha were employed to observe the relationship between cervical cancer and prolactin. By immunocytochemical and indirect immunofluorescent assays using two prolactin monoclonal antibodies PRL-149 and PRL-151, both cell lines with added prolactin (10 ng/mL) were noted to be positive for PRL-151, but negative for PRL-149. The control cell lines from ovarian cancer and the myeloma lines were both stained negative. By using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, it was noted that CC7-T and Si-Ha grew better in the presence of various added concentrations of prolactin, ranging from 0.1 to 1,000 ng/mL, suggesting that prolactin may enhance the growth of cervical cancer. The degree of stimulation appears to depend on cell differentiation. However, prolactin levels in the cultured supernatant were undetectable by the enzyme immunoassay (EIA) method. We postulate that prolactin can bind and stimulate the growth of some cervical cancer cell lines, probably through the prolactin receptor rather than by autocrine regulation.

Animals↗
PubMed1992

Stimulation by risperidone of rat prolactin secretion in vivo and in cultured pituitary cells in vitro.

Risperidone, a new antipsychotic agent which antagonizes both 5-hydroxytryptamine-2 (5-HT2) and dopamine-2 (D2) receptors, was evaluated for its effects on prolactin release. One hr after either p.o. or i.p. dosing, risperidone was 3 to 5 times more potent than the classical D2 receptor antagonist haloperidol in stimulating rat prolactin levels in vivo. This result was unexpected because haloperidol is a more potent D2 receptor antagonist than risperidone in vitro. Mechanisms which might explain these observations were investigated. Compared to haloperidol, risperidone was 0.34 (95% confidence interval: 0.23, 0.48) times as potent in reversing the suppression by dopamine of rat anterior pituitary cell prolactin release in vitro, which is consistent with the compounds' striatal D2 receptor binding potencies in vitro. Administration of ketanserin, a 5-HT2 receptor antagonist, along with haloperidol did not modify haloperidol's activity on either in vitro pituitary cell prolactin release (up to 1000 nM ketanserin) or in vivo prolactin concentrations (5 mg/kg ketanserin, i.p.). In vitro incubation of haloperidol and risperidone with a liver homogenate supernatant (S-9) led to extensive (greater than 86%) metabolism of each compound. S-9 treatment abolished haloperidol's effects on pituitary cell prolactin release. Risperidone's ability to increase prolactin release was unchanged after S-9 treatment, and 9-hydroxy-risperidone, identified as a major metabolite in the S-9 conditioned media, was equipotent to risperidone in modulating prolactin release in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗