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PubMed1985

Differential effects of prolactin on rat dorsolateral prostate and R3327 prostatic tumor sublines.

Many investigators have reported effects of the pituitary hormone, prolactin, on the physiology and biochemistry of the rat prostate gland, particularly the lateral or dorsolateral lobe. The Dunning R3327H is a transplantable rat prostatic adenocarcinoma derived from a spontaneous tumor of the Copenhagen rat dorsolateral prostate. This study describes and compares morphological and physiological effects of prolactin on rat dorsolateral prostate and two sublines of the Dunning tumor. Ectopic pituitary grafts were used to induce chronic hyperprolactinemia in castrated rats receiving androgen supplement to provide a relatively controlled hormonal environment in which the effects of prolactin were maximally and consistently observed. Gravimetric and biochemical analyses, as well as ultrastructural study, provided evidence of prolactin's stimulatory effect on dorsolateral prostate growth and secretory activity. Hyperprolactinemia stimulated the growth of the well-differentiated, androgen-dependent R3327/3219 tumor subline with an increase in weight, volume and the total content of DNA, protein and zinc. There were no changes in tumor morphology. In contrast, the anaplastic androgen-independent R3327/150 tumor subline did not respond to graft-induced hyperprolactinemia. This differential response of the two R3327 tumor sublines attests to the complexity of prolactin's effects on prostatic tissue and to the extent of the deterioration of endocrine control that often accompanies tumor progression. Prolactin binding in the R3327 sublines was studied using immunohistochemical staining and radioligand assay, but produced complex results which raise questions about the discrepancy between hormone binding and biological action of prolactin in prostatic tissues.

Adenocarcinoma↗
PubMed1998

Expression of prolactin messenger ribonucleic acid in the mouse gonads during sexual maturation.

The pituitary hormone prolactin is known to be produced in various extrapituitary tissues as well. We examined the presence of prolactin mRNA in the mouse gonads by reverse transcription (RT)-PCR and nucleotide sequence analysis. Both ovary and testis were found to express small amounts of mRNA coding prolactin, identical to that in the pituitary gland. Next, we established a sensitive competitive RT-PCR method to estimate the amount of prolactin mRNA and then measured its expression in the gonads during sexual maturation (10-80 days of age). In the ovary, the amount of prolactin mRNA (copies/microg of total RNA) gradually decreased from day 10 to 40, and the lower level was maintained until day 80. Little difference in the amount was observed between the estrous and diestrous groups on day 80. Conversely, the amount of testicular prolactin mRNA gradually increased from day 10 to 80. These results suggest that prolactin is produced in the mouse gonads and that it acts as an autocrine/paracrine factor modulating gonadal functions.

Animals↗
PubMed1996

Prolactin and beta-endorphin responses to hypoglycemia are reduced in well-controlled insulin-dependent diabetes mellitus.

Several pituitary hormones, including corticotropin (ACTH), growth hormone (GH), prolactin, and beta-endorphin (but not thyrotropin, follicle-stimulating hormone, or luteinizing hormone), are released in response to hypoglycemia in normal subjects. In patients with insulin-dependent diabetes mellitus (IDDM), the degree of glycemic control is known to alter ACTH and GH responses to hypoglycemia. The current study was performed to examine the effect of glycemic control on prolactin and beta-endorphin responses to hypoglycemia in subjects with IDDM. We performed 3-hour stopped hypoglycemic-hyperinsulinemic clamp studies (12 pmol/kg/min) during which plasma glucose was decreased from 5.0 mmol/L to 2.2 mmol/L in steps of 0.6 mmol/L every 30 minutes in 20 subjects with uncomplicated IDDM (12 males and eight females; age, 26 +/- 2 years; IDDM duration, 10 +/- 1 years; body mass index, 23.6 +/- 0.6 kg/m2) and 10 healthy subjects (five males and five females aged 30 +/- 1 years). The 10 diabetic subjects in good glycemic control (mean hemoglobin A1 [HbA1], 7.5% +/- 0.3%; normal range, 5.4% to 7.4%) were compared with the 10 poorly controlled patients (mean HbA1, 12.6% +/- 0.5%; P < .001 v well-controlled diabetic group). During hypoglycemia, prolactin levels in the well-controlled diabetic group did not change (7 +/- 1 microgram/L at plasma glucose 5.0 mmol/L to 9 +/- 2 micrograms/L at plasma glucose 2.2 mmol/L), whereas prolactin levels increased markedly in the poorly controlled diabetic group (7 +/- 2 micrograms/L to 44 +/- 17 micrograms/L) and healthy volunteers (12 +/- 2 micrograms/L to 60 +/- 19 micrograms/L, P < .05 between IDDM groups). The plasma glucose threshold required for stimulation of prolactin secretion was 2.2 +/- 0.1 mmol/L in well-controlled IDDM, 3.0 +/- 0.4 mmol/L in poorly controlled IDDM, and 2.4 +/- 0.1 mmol/L in healthy subjects (P < .05 between IDDM groups). Responses in males and females were similar. The increase in beta-endorphin levels was also attenuated in well-controlled IDDM patients (4 +/- 1 pmol/L at plasma glucose 5.0 mmol/L to 11 +/- 4 pmol/L at plasma glucose 2.2 mmol/L) versus poorly controlled IDDM patients (5 +/- 1 pmol/L to 26 +/- 7 pmol/L) and healthy subjects (8 +/- 1 pmol/L to 56 +/- 13 pmol/L). The plasma glucose threshold required for stimulation of beta-endorphin release was again lower in well-controlled IDDM versus poorly controlled IDDM patients (2.2 +/- 0.1 v 3.0 +/- 0.3 mmol/L) and healthy subjects (2.5 +/- 0.4 mmol/L, P < .05 between IDDM groups). In conclusion, prolactin and beta-endorphin responses to a standardized hypoglycemic stimulus (plasma glucose, 2.2 mmol/L) are reduced and plasma glucose levels required to stimulate release of prolactin and beta-endorphin are lower in well-controlled IDDM compared with poorly controlled IDDM and healthy subjects. Thus, stress hormones not previously considered to have a primary role in plasma glucose recovery from hypoglycemia are affected by glycemic control, suggesting a more generalized alteration of hypothalamic-pituitary responses to hypoglycemia in IDDM patients with strict glycemic control.

Adult↗
PubMed2000

Depot medroxyprogesterone acetate and basal serum prolactin levels in lactating women.

OBJECTIVE: To study the effect of depot medroxyprogesterone acetate on basal serum prolactin levels in lactating women. METHODS: We compared basal serum prolactin levels in 25 lactating women after depot medroxyprogesterone acetate injection and in 25 lactating women of similar age who were using a copper T380A intrauterine device (control group). This sample size was required in order to have 95% power to detect a significant difference. Basal prolactin levels were evaluated by time-resolved fluoroimmunoassay three times (6 weeks postpartum and 3 and 6 weeks after beginning either contraceptive method). RESULTS: At 6 weeks postpartum, before beginning either contraceptive method, the mean prolactin levels in the study and control groups were 991.31 and 948.75 mU/L, respectively (P =.850, 95% confidence interval [CI] -407.57, 492.70). Three weeks later, the mean prolactin levels in the study and control groups were 1156.12 and 860.10 mU/L, respectively (P =.116, 95% CI -76.20, 668.26). At the last follow-up, the mean prolactin levels in the study and control groups were 1127.83 and 710.97 mU/L, respectively (P =.026, 95% CI 51.97, 781.73). There were no significant within-group differences at 6 weeks postpartum before contraception and at 6 weeks after beginning contraception in the study and control groups (P >.05, 95% CI -327.99, 243.02 and -46.76, 522.33, respectively). CONCLUSION: Contraception with depot medroxyprogesterone acetate in lactating women produced higher basal prolactin levels than contraception with copper T380A intrauterine device.

Contraceptive Agents, Female↗
PubMed2001

Prolactin levels are elevated after infant carrying in parentally inexperienced common marmosets.

Alloparental behavior (parental behavior directed to nondescendant young) is pervasive among human cultures but rare among other mammals. New World primates of the family Callitrichidae, including common marmosets (Callithrix jacchus jacchus), dwell in large families and many family members carry and/or provision infants. This study experimentally characterized alloparenting in common marmosets by measuring infant retrieval and carrying outside of the context of the family group. Prolactin was measured in samples collected before and after infant exposure to determine whether elevated prolactin levels were predictive of alloparental responsiveness. Seventeen nonbreeding, parentally inexperienced, singly or peer-housed common marmosets (10 females, 7 males, 6-66 months of age) were tested repeatedly in an infant retrieval paradigm. Infant retrieval was shown by 5 out of 17 monkeys (29%) in their first test. The rate of retrieval increased to 10 monkeys (59%) by the fourth test. No significant differences in age, sex, or housing condition existed between monkeys that retrieved infants and those not retrieving. Prolactin concentrations were significantly elevated in serum obtained after testing only in monkeys that retrieved infants. Prolactin levels after infant exposure were positively related to carrying duration. A separate experiment verified that neither prolactin nor cortisol was significantly elevated in response to prolonged handling. Cortisol levels were inversely proportional to handling time. Prolactin levels were not significantly related to handling time. Our results indicate that alloparental behavior is expressed at high rates after minimal infant experience, and prolactin levels rise concomitantly with the expression of alloparental behavior in this species.

Aging↗
PubMed1988

Immunoreactive prolactin in lesions and tumours of salivary glands.

The prolactin binding in obstructive lesions and tumours of salivary glands was described by use of the immunohistochemical PAP technique. Normal salivary glands had prolactin binding cells in the striated ducts only. Chronic obstructive lesions of submandibular glands showed negative immunoreaction for prolactin binding in ductal cells, but positive staining of the luminal surface of ductal segments. In pleomorphic adenomas, occasional neoplastic cells located along the luminal borders of tubular, ductal, or of duct-like epithelial structures were strongly reactive with anti-prolactin and 26.5% of cases pleomorphic adenoma were positive for anti-prolactin. Adenoid cystic carcinoma exhibited positive prolactin binding on the luminal surface of some of tumour foci, but not in the rest of the tumour. Warthin's tumour was devoid of detectable prolactin binding.

Humans↗
PubMed1979

Tests of prolactin secretion in diagnosis of prolactinomas.

Prolactin-secreting tumours of the pituitary were identified and treated by transsphenoidal microsurgery in fourteen infertile females with hyperprolactinaemia. Resting prolactin levels were 590--9000 mU/1 (mean 3400). In seven patients, tomography of the pituitary fossa was normal and resting prolactin levels were 590-6000 mU/1 (mean 3400). In these patients the pre-operative diagnosis prolactinoma in these patients was made by demonstrating loss of the normal circadian prolactin profile and impaired prolactin response to intravenous thyrotrophin-releasing hormone (T.R.H.) and metoclopramide stimulation. Prolactin response to the acute oral administration of L-dopa and bromocriptine was of less diagnostic value. Preoperative assessment of anterior pituitary function identified abnormalities other than hyperprolactinaemia in four patients (28%). Post-operative assessment indicated that microsurgery was curative in twelve patients (86%), selective in all, and without significant side-effect. It is concluded that dynamic tests such as T.R.H. and metoclopramide stimulation have considerable value in identifying hyperprolactinaemic patients with prolactin-secreting adenomas, particularly those which are radiologically occult.

Adolescent↗
PubMed2001

Coitus-induced orgasm stimulates prolactin secretion in healthy subjects.

Previous data have indicated that orgasm produces marked alterations in plasma prolactin concentrations in men and women. Thus, the current study aimed to extend these data by examining prolactin response to coitus in healthy males and females. Ten pairs of healthy heterosexual couples participated in the study. Blood was drawn continuously for 20 min before, during, and until 60 min following sexual intercourse and orgasm. Plasma was subsequently analysed for prolactin concentrations. Coitus-induced orgasm produced a marked elevation of plasma prolactin in both males and females. Plasma prolactin concentrations remained elevated 1 h following orgasm. These data, together with previous evidence that masturbation-induced orgasm produces pronounced, long-lasting increases in plasma prolactin concentrations in both males and females, suggest a role for acute prolactin alterations in modifying human sexual desire following orgasm.

Adult↗
PubMed2000

Evidence for a seasonal variation in the ability of exogenous melatonin to suppress prolactin secretion in the mare.

In seasonally breeding species photoperiodic information is thought to be conveyed to the reproductive and prolactin axis via changes in circulating concentrations of melatonin. For some species, a constant melatonin stimulus is perceived as a short day, whereas in others no photoperiodic information is provided. In the mare, a preliminary study demonstrated that constant administration of melatonin did not modify prolactin secretion, suggesting that this treatment regimen failed to provide photoperiodic information. To further investigate this proposal and to investigate an alternative explanation, namely a seasonal variation in response to melatonin, 4 experiments were performed. In experiments 1-3, the effects of constant administration of melatonin on prolactin secretion were investigated. In each study the time of treatment initiation varied beginning before the summer solstice, (May 9; Exp. 1), at the autumnal equinox (Sept. 21; Exp. 2) or the winter solstice (Dec. 21; Exp. 3). In Experiment 4, melatonin was administered as a timed daily injection (5 PM) for 6 months, beginning at the summer solstice (June 21). Constantly elevated physiological concentrations of melatonin (expts. 1-3) and an extended nighttime elevation of melatonin (exp. 4) suppressed prolactin concentrations only during the spring and early summer months (April-August). At other times during the year prolactin concentrations were similar to untreated mares. In the presence of a continuous melatonin implant the circannual rhythm of prolactin secretion was not disturbed. The results suggest that the prolactin axis of the mare is sensitive to an inhibitory melatonin signal during a restricted period of time and that at other times is refractory to this signal.

Animals↗
PubMed1999

Prolactin and insulin levels in lactating sows in relation to nursing frequency.

It has been established that sows up- or down-regulate their milk production as the frequency of nursings is changed. The amount of udder massage by piglets might also influence milk production. To investigate whether these effects are associated with changes in prolactin or insulin levels, we enforced five sows each to nurse either every 35 min (MIN35) or every 70 min (MIN70) over a 26- to 28-hr period. Milk production was measured during the first 24 hr of this period. During the last three to four nursings, blood was collected every 5 min. Plasma prolactin levels increased after milk ejection (P < 0.05), whereas insulin levels increased only briefly in MIN70 sows. Sows nursing every 35 min had lower basal (P < 0.001) and maximal (P < 0.05) concentrations of insulin than MIN70 sows. There were no differences between the two groups in prolactin levels. Nursings with a postejection udder massage longer than 90 s tended to induce a higher increase in prolactin (P < 0.1) than nursings with a shorter massage. When the effects of imposed nursing frequency were removed, there was an across-sows positive residual correlation between average prolactin levels (P < 0.05) and the duration of post-ejection udder massage during the preceding 24 hr. We conclude that when milk production of a sow is changed by altering the nursing frequency within natural limits, the necessary alteration in catabolic state of energy metabolism may be associated with altered insulin levels. The duration of udder massage in a single nursing might have only a slight immediate impact on prolactin levels, but may influence prolactin levels more substantially if increased for a period of 24 hr.

Animals↗
PubMedDate not supplied

Sulpiride-induced increases in serum prolactin levels in female rats exposed prenatally to alcohol.

We examined the impact of prenatal alcohol exposure on serum prolactin levels and on the ability of the D2 dopamine antagonist sulpiride to stimulate prolactin release in Long-Evans rats. Pregnant rats were intubated with alcohol (0, 3, or 5 g/kg/day) from gestational day 8 (GD8) to GD20. Adult female offspring were screened for estrous cycle stage. At diestrus, the rats were challenged with a single dose of sulpiride (0, 10, or 40 micrograms/kg) and trunk blood was collected 20 min later. After prenatal exposure to either dose of alcohol, mean basal serum levels of prolactin were about 65% less than the 0 g/kg group, and the 35-40% mean differences from an untreated control group were not significant. Sulpiride produced dramatic dose-dependent increases in serum prolactin levels in all prenatal treatment groups. Across all doses of sulpiride, the group given the higher dose of prenatal alcohol (5 g/kg/day) had significantly lower serum prolactin levels than all other groups. There was no significant interaction between prenatal treatment and sulpiride dose. Neither prenatal alcohol exposure nor sulpiride injections had significant effects on serum corticosterone levels in this study. Although the current results are unclear regarding a baseline decrease in prolactin levels after prenatal alcohol exposure, the overall results suggest that prenatal alcohol exposure decreases prolactin levels but there is no evidence that it does so by altering dopaminergic tone in hypothalamus of female rats.

Animals↗
PubMed2001

Estrogen, prolactin, and autoimmunity: actions and interactions.

Estrogen and prolactin have a reciprocal endocrinologic relationship and both hormones have pleiotropic effects on the immune system. Despite the presence of a number of confounding variables, these hormones modulate autoimmunity; however, mechanisms by which this modulation occurs remain obscure. Estrogen appears to suppress cell-mediated and augment humoral-based immunity. Prolactin appears to stimulate both cell and humoral-based immunity. Both hormones have been shown to modulate IFN gamma secretion. Similar evidence in experimental models, human autoimmune disease, and during pregnancy in autoimmune disease patients suggests disparate effects of estrogen and prolactin on autoimmune responses and disease pathogenesis. In the NZB x NZW F1 mouse model of lupus, prolactin accelerates disease expression, whereas estrogen, devoid of its prolactin stimulating properties, is immunosuppressive and inhibits IL-2 production. Estrogen, because of its endocrinologic and immune effects, may directly or indirectly stimulate or inhibit immune responses. These dichotomous effects have limited its successful pharmacologic manipulation in human autoimmune disease with estrogen compounds, tamoxifen, oral contraceptives, antigonadotropic agents, or ovulation induction regimens. In contrast, reduction of immunostimulatory concentrations of prolactin with bromocriptine has successfully suppressed development or expression of murine and human autoimmune disease. Further investigation into actions and interactions of estrogen and prolactin with autoimmunity will provide a better understanding of the female preponderance of autoimmunity and facilitate a more rational approach to hormonal immunotherapy.

Animals↗
PubMed1993

Bromocriptine treatment of periparturient goats: long-term suppression of prolactin and lack of effect on lactation.

British Saanen dairy goats (n = 10) were treated with bromocriptine or vehicle from day 147 of pregnancy to day 4 post partum, a treatment duration of 8.8 +/- 1.7 d (mean +/- SEM). The periparturient prolactin surge was abolished by this treatment, but there were no significant effects on plasma growth hormone or insulin concentrations. Lactogenesis was delayed in the bromocriptine-treated goats, milk yields being significantly depressed (P < 0.01) for the first week of lactation. Yields had recovered to control values by day 10 when prolactin concentrations were still significantly depressed. Mammary gland biopsies were taken on day 4 post partum from five animals in each group. Using this tissue, no significant differences could be shown in mammary morphology or DNA synthesis, but the RNA:DNA ratio was significantly reduced (P < 0.05). After week 1, there were no significant differences between bromocriptine-treated and control goats in milk yield, milk composition, udder volume, time of peak yield or persistence. The goats given short-term bromocriptine treatment at parturition showed prolonged effects on prolactin secretion, their seasonal prolactin rise being severely blunted (P < 0.001). A normal lactation is therefore not prevented in goats by a delay in lactogenesis, suppression of prolactin at parturition or the resulting prolonged depression of circulating prolactin. Goats in established lactation given bromocriptine for 8 d showed, by contrast, a rapid recovery of plasma prolactin concentrations within 5 d post treatment. Milk yield declined significantly (P < 0.03) compared with pretreatment values during and for 1 week after bromocriptine but then began to recover, with no significant change in vehicle-treated goats.

Animals↗
PubMed1998

Cadmium does not inhibit pulsatile prolactin secretion through TRH.

This work was undertaken to analyse the effects of acute cadmium administration on the pulsatile pattern of prolactin release, in adult male rats. For this purpose, animals were cannulated 40 h before the experiment to allow a continuous blood withdrawal. Two hours after the administration of one dose of cadmium chloride (4.5 mg kg1), the pulsatile pattern of prolactin, during three hours, was studied. The effects of two pulses of thyrotropin-releasing hormone (TRH) (1 microgram per rat), given 60 and 120 min after starting the period of blood sampling, were studied. The mean values of prolactin during the bleeding period and the absolute pulse amplitude were decreased by acute cadmium chloride administration. However, no changes in any other parameters of prolactin pulsatility were observed. TRH administration to control rats increased mean prolactin levels, and absolute and relative pulse amplitudes, but decreased the mean half-life of the hormone. In animals pretreated with cadmium, TRH increased the mean levels of prolactin, and absolute and relative amplitudes of the hormone pulses. No other parameter studied was changed by TRH in cadmium pretreated rats. These data suggest that acute administration of cadmium did not inhibit the pulsatile prolactin release through TRH.

Animals↗
PubMed2002

The effects of atypical antipsychotics on serum prolactin levels.

Hyperprolactinemia may be a concern in the treatment of patients with schizophrenia. The side effects associated with high prolactin levels can have a negative impact on patient compliance with treatment. Atypical antipsychotics as a group cause less hyperprolactinemia than conventional antipsychotics, yet there is considerable variation among specific drugs. Risperidone at higher doses has been shown to produce increases in prolactin similar to conventional antipsychotics. At the other end of the spectrum, clozapine and quetiapine produce minimal sustained increases in prolactin that are no different from placebo. However, correlations between prolactin elevations and clinical symptoms have not been well-established. This paper reviews the published literature regarding prolactin levels in treated and untreated patients with schizophrenia and the relationship of prolactin and dopamine. It concludes with an overview of the effects of specific atypical antipsychotics on prolactin levels in patients with schizophrenia.

Antipsychotic Agents↗
PubMedDate not supplied

Discrete cis-active genomic sequences dictate the pituitary cell type-specific expression of rat prolactin and growth hormone genes.

The anterior pituitary gland, which is derived from a common primordium originating in Rathke's pouch, contains phenotypically distinct cell types, each of which express discrete trophic hormones: adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), prolactin, growth hormone, and follicle stimulating hormone (FSH)/luteinizing hormone (LH). The structurally related prolactin and growth hormone genes, which are evolutionarily derived from a single primordial gene, are expressed in discrete cell types--lactotrophs and somatotrophs, respectively--with their expression virtually limited to the pituitary gland. The pituitary hormones exhibit a temporal pattern of developmental expression with rat growth hormone and prolactin characteristically being the last hormones expressed. The reported co-expression of these two structurally related neuroendocrine genes within single cells prior to the appearance of mature lactotrophs, in a subpopulation of mature anterior pituitary cells, and in many pituitary adenomas raises the possibility that the prolactin and growth hormone genes are developmentally controlled by a common factor(s). We now report the identification and characterization of nucleotide sequences in the 5'-flanking regions of the rat prolactin and growth hormone genes, respectively, which act in a position- and orientation-independent fashion to transfer cell-specific expression to heterologous genes. At least one putative trans-acting factor required for the growth hormone genomic sequence to exert its effects is apparently different from those modulating the corresponding enhancer element(s) of the prolactin gene because a pituitary 'lactotroph' cell line producing prolactin but not growth hormone selectively fails to express fusion genes containing the growth hormone enhancer sequence.

Animals↗
PubMed1987

Presence and possible significance of immunohistochemically demonstrable prolactin in breast apocrine metaplasia.

Paraffin wax embedded formalin-fixed benign breast disease tissue taken from 17 patients (15 with microcystic disease and 2 with fibroadenoma) was studied for the presence of tissue bound prolactin using a rabbit antiserum against human prolactin applied in conjunction with a highly sensitive modified version of the dinitrophenyl (DNP)-hapten sandwich staining (DHSS) procedure. Sections taken from 14 of the 15 cases showing apocrine cystic changes exhibited strong prolactin staining restricted to the cytoplasm of metaplastic apocrine cells lining the cysts. Normal lobules and ducts and blunt duct proliferations were all negative, as were also the two cases of fibroadenoma. In contrast 6 out of 8 cases of breast cancer examined showed heterogenously distributed cytoplasmic staining in the cancer cells. Maximal prolactin staining in the apocrine cells was observed at antiserum dilutions as high as 1:60,000. This compared favourably with a 1:120,000 dilution that gave maximal levels of staining in the prolactotrophs present in serial sections taken from formalin fixed paraffin wax embedded post mortem human anterior pituitaries. In both types of tissues the specific staining was abolished by pre-absorption of the antiserum with human prolactin (10 micrograms ml-1). No staining was observed when the anti-prolactin serum was either omitted or substituted with DNP-labelled normal rabbit serum. Apocrine metaplasia in cystic disease of the breast has recently been found to be associated with an increased breast cancer risk. The strong and selective presence of immunohistochemically demonstrable prolactin in the metaplastic cells may be of significance in view of the hormone's known growth stimulating effect on the breast epithelium.

Adenofibroma↗
PubMed1987

Intravenous medroxalol stimulates prolactin secretion in normal and hypertensive subjects.

This study evaluated the effects of medroxalol on prolactin secretion. Twelve normal subjects received medroxalol, 1 mg/kg, intravenously and on a separate occasion, 5% dextrose in water. Integrated prolactin secretion during the 3 hours after medroxalol injection was significantly increased as compared with dextrose (P less than 0.001). Intravenous administration of medroxalol, 2 mg/kg, to 10 hypertensive subjects resulted in significant elevation of mean prolactin levels above basal levels at all time intervals measured from 30 to 240 minutes after injection. Oral medroxalol administration to 11 hypertensive subjects for up to 15 months did not alter mean prolactin levels. Medroxalol neither stimulated prolactin release nor decreased dopamine suppression of prolactin release from pituitary cell cultures. In conclusion, intravenous medroxalol stimulates prolactin secretion in both normal and hypertensive subjects. This effect is not likely mediated by a direct action of the drug on the pituitary but rather by an effect either within the central nervous system or of a drug metabolite.

Adult↗