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PubMed2000

Adrenoceptor subtype involvement in suppression of prolactin secretion by noradrenaline.

In sheep, injection of noradrenaline suppresses prolactin secretion by a direct effect at the pituitary gland. The aims of this study were to use primary cultures of ovine pituitary cells to examine the receptor subtypes that mediate the inhibitory effect of noradrenaline on prolactin secretion and, by using receptor antagonists in vivo, determine whether noradrenaline acts as a prolactin release-inhibiting factor (PIF). Noradrenaline and dopamine suppressed prolactin secretion from ovine pituitary cells with ED50s of 60.9+/-46.6 and 1.5+/-1.0x10-9 mol/l, respectively (P<0.05). The in-vitro prolactin release-inhibiting effect of noradrenaline (10-7 mol/l) was not blocked by the dopamine antagonists pimozide (D2) or SCH23390 (D1) but was blocked by each of the adrenoceptor antagonists (alpha1-adrenoceptor antagonists prazosin and WB4101, the alpha2-adrenoceptor antagonist yohimbine and the beta-adrenoceptor antagonist propranolol). The response to adrenoceptor agonists was also tested in vitro. The alpha1-adrenoceptor agonists phenylephrine and cirazoline significantly suppressed prolactin. Of the alpha2-agonists, clonidine had no effect whereas oxymetazoline and p-aminoclonidine both suppressed prolactin. The beta-adrenoceptor agonist isoproterenol also suppressed prolactin while the specific beta3-antagonist BRL37344 had no effect. When the adrenoceptor antagonists were tested in vivo in ewes manipulated to be in the luteal phase, only WB4101 significantly (P<0.05) increased plasma prolactin concentrations but this response was small and only observed in one of two experiments. In summary, these experiments suggest that adrenoceptors and not dopamine receptors are responsible for the inhibitory effect of noradrenaline on prolactin secretion in vitro but do not implicate a particular adrenoceptor subtype. The in-vivo experiments do not provide convincing evidence for a role for noradrenaline as a physiologically important PIF.

Adrenergic Agonists↗

PubMed2001

Stimulating effect of glycoprotein hormone free alpha-subunit and daily gonadotropin releasing hormone treatment on prolactin release from 50-day ovine foetal pituitary explants.

The aim of our study was to determine whether free alpha of glycoprotein hormones (free alpha) plays a role in lactotroph function during early pituitary development in the sheep foetus. Detection and quantification of free alpha, luteinzing hormone beta-subunit (LHbeta) and prolactin immunolabelling were determined by immunocytochemistry at days 32, 37, 42, 50 and 63 of gestation. Free alpha- and LHbeta-containing cells were first detected in the ovine foetal pituitary gland on day 37 of gestation, while prolactin-containing cells were first identified on day 42. Analysis of serial sections suggested that free alpha immunoreactive cells were also LHbeta-positive, indicating that free alpha was mainly synthesized by gonadotrophs. In early foetal stages, free alpha occurred in the antero-medio ventral region of the pituitary gland, whereas prolactin-containing cells were more dorsally and more caudally localized. The free alpha-, LHbeta- and prolactin-immunostained area increased markedly between days 50 and 63 of gestation. To evaluate a possible functional relationship between gonadotrophs and lactotrophs, the effects of free alpha or gonadotropin releasing hormone (GnRH) on prolactin release were assayed. Chronic treatment of pituitary explants from male and female 42-day-old ovine foetuses for 8 days with 10-9 or 10-7 M ovine free alpha did not affect prolactin release. By contrast, free alpha administration on pituitary explants from male and female 50-day-old foetuses resulted in enhanced prolactin release. At this age, a daily (2 h per day) treatment with 10-8 M GnRH had similar stimulatory effect to free alpha whereas a 'first day' treatment (24 h on the first day) reduced prolactin release throughout the culture in males and had no effect in females. These results indicate that, despite early detection of free alpha at day 37 in the ovine foetal pituitary, its stimulatory effect on prolactin release occurs from day 50 of gestation, corresponding to the first period of lactotroph development in vivo. A daily treatment with GnRH mimics the effect of free alpha on prolactin release.

Animals↗

PubMed1987

The prolactin response to TRH and domperidone does not differentiate male hypothalamic hypogonadism and constitutional delay of puberty.

In order to test whether prolactin response to challenge with TRH and domperidone, dopamine receptor antagonist, is diagnostic for idiopathic hypothalamic hypogonadism (IHH) we studied 8 normal controls, 9 subjects with delayed sexual development and 6 patients with IHH. TRH test (200 micrograms i.v. bolus) and domperidone (10 mg i.v. bolus) were given on two different days. Prolactin (RIA-Biodata) was determined in blood samples during the test. The basal value of prolactin in subjects with delayed puberty and healthy controls did not differ from basal values of prolactin in patients with IHH. The peak elevation of prolactin after TRH in subjects with delayed puberty and healthy controls did not differ from that in patients with IHH. After successful treatment of one patient with IHH (Kallmann's syndrome) with pulsatile s.c. LHRH we did not find any change in the response of prolactin to TRH challenge after 1, 3 and 6 months of treatment, while prolactin response to domperidone increased. Prolactin responses to TRH and domperidone are not differential for the early diagnosis of IHH. Successful treatment of a patient with IHH did not change the response of prolactin to TRH, but increased prolactin response to domperidone possibly due to altered steroid milieu.

Adolescent↗

PubMed1989

Role of milk secretion in transport of prolactin from blood into milk.

In a first experiment prolactin was shown to be uniformly distributed in the milk of dairy cows. Accumulation of prolactin in milk increased with milking interval although milk prolactin content was proportionally greater after 2 h than accumulation of milk. Concentration of milk prolactin and total transfer of prolactin into milk was greater in mammary glands of cows milked just prior to initiation of intravenous infusion of exogenous prolactin. Similarly, inhibition of milk secretion as induced by intramammary infusion of colchicine, markedly reduced milk prolactin concentration and total transfer of prolactin into milk 5h following start of intravenous infusion of exogenous prolactin. Data indicate that transfer of prolactin from blood into milk during established lactation occurs primarily in conjunction with milk secretion.

Animals↗

PubMed1980

Dose-dependency and reproducibility of the prolactin response to metoclopramide.

Six normal volunteers were tested to ascertain the dose-dependency and reproducibility of the prolactin response to metoclopramide. Furthermore, pretreatments with 1-dopa or cyproheptadine were performed. The same subjects also received intravenously 500 microgram TRH. The oral administration of 5 mg metoclopramide produced a significant rise in prolactin at 60 min and a maximal elevation at 90 min. The intravenous administration of 5 mg metoclopramide produced a significant increment at 15 min and a maximal prolactin level at 30 min. Peak prolactin levels following i.v. administration of the drug were greater than those after oral administration. Intravenous administration of 1 mg of metoclopramide produced a potential increment in plasma prolactin. Maximal prolactin response to 1 mg i.v. metoclopramide was similar to that found with 500 microgram i.v. TRH. Reproducibilities of prolactin response were good in all doses and modes of administration of metoclopramide. Pretreatment with 1-dopa inhibited the metoclopramide-induced prolactin response, but pretreatment with cyproheptadine did not influence the prolactin response to metoclopramide. Metoclopramide is a good and reproducible stimulator of prolactin secretion.

Adult↗

PubMed1995

Mutation of serine 90 to glutamic acid mimics phosphorylation of bovine prolactin.

Phosphorylated prolactin has been identified and isolated from bovine pituitaries. The biological activity of this phosphoprotein is severely reduced in comparison with nonphosphorylated prolactin. The sites of phosphorylation are serines 26, 34, and 90, and the stoichiometry is 1:1:10, respectively. In this report, the phosphoserine residues have been individually replaced with glutamic acid in recombinant methionyl bovine prolactins in order to mimic phosphorylation at each site. Substitution of glutamic acid for serine at positions 26, 34, and 90 reduced protein helical contents by 10, 6, and 14%, respectively. UV absorbances for S26E and S34E bovine prolactins were blue-shifted, similar to the biological isolates of phosphorylated bovine prolactin, but the biological activities of the S26E and S34E mutants (ED50 values of 16.3 and 18.8 pM, respectively) were similar to that of wild-type prolactin (ED50 value of 18.6 pM) in the Nb2 rat lymphoma assay. S90E bovine prolactin had the greatest reduction in helical content but showed similar UV and fluorescent spectra to the wild-type bovine prolactin. The biological activity of S90E bovine prolactin (ED50 value of 672 pM) was reduced to an activity similar to that of phosphorylated bovine prolactin. The data indicate that the phosphorylation of serine 90 is responsible for the reduction in biological activity.

Amino Acid Sequence↗

PubMed1992

Effect of reserpine on the inhibition of prolactin released from different pituitary constructs in vitro by dopamine, bromocriptine and apomorphine.

Hourly release of Prolactin by pituitary constructs 1 whole pituitary (PI), adenohypophysis (P-N) and pituitary-hypothalamus co-incubate (PHC) were compared. Adenohypophysis secreted significantly more prolactin than PI and PHC, while PHC secreted significantly less than PI. Co-incubation of (P-N) with posterior pituitary reduced the elevated secretion of prolactin. Addition of dopamine (10(-7) M), bromocriptine (10(-7) M) and apomorphine (5 x 10(-8) M) to these constructs did not affect the release of prolactin from PI but inhibited the same from (P-N) and PHC. Treatment with reserpine increased serum prolactin levels but intrapituitary prolactin contents were decreased. Hourly release of prolactin from pituitary constructs derived from reserpine-treated rats was significantly reduced as compared to ascorbic acid--treated controls. Inclusion of dopamine (10(-7) M), bromocriptine (10(-7) M) and apomorphine (5 x 10(-8) M) in these constructs inhibited prolactin secretion further. In vitro addition of perphenazine stimulated the release of prolactin by PHC but was without any effect on PI and (P-N). The data are interpreted to suggest that dopamine in posterior pituitary may be an important determinant of hypothalamic modulation of prolactin secretion.

Animals↗

PubMed2002

The brain prolactin system: involvement in stress response adaptations in lactation.

This review focuses on prolactin as a potential candidate for the regulation of emotional and neuroendocrine stress responses in the brain. In particular, we summarise evidence for a brain prolactin receptor-mediated anxiolytic action both in female and male rats, and for inhibitory actions on the reactivity of the hypothalamic-pituitary-adrenal (HPA) axis and the neurohypophysial oxytocin system. These physiological functions of the brain prolactin system are especially relevant in the peripartum period, as an attenuation of behavioural and neuroendocrine stress responses has been described during pregnancy and lactation. At this time, there is an increase in brain prolactin receptor expression and binding, and an increase in hypothalamic prolactin gene expression. In the absence of a selective prolactin receptor antagonist, complementary approaches including chronic intracerebral infusion of prolactin, and antisense targeting of the long form of the brain prolactin receptor were used to investigate the actions of prolactin. The hypothesis of a brain prolactin system activated in the peripartum period which contributes to the adaptive changes in stress responsiveness in order to support reproductive functions is strongly emphasised.

Adaptation, Physiological↗

PubMed1981

Cloning of bovine prolactin cDNA and evolutionary implications of its sequence.

Prolactin, growth hormone, and chorionic somatomammotropin (placental lactogen) constitute a set of related polypeptides believed to derive from a common evolutionary ancestor protein. We have cloned and sequenced DNA complementary to the mRNA coding for bovine prolactin. This cDNA contains 702 bases corresponding to 10 amino acids in the leader peptide, all 199 amino acids of the hormone, and 75 nucleotides in the 3' untranslated region of the mRNA. Nucleotide sequence analysis of this cDNA permitted the identification of 10 amino acids in the signal peptide, plus the correction or elucidation of amino acid assignments at 16 sites where aspartic and glutamic acids had not been distinguished from their amides by amino acid sequencing. Codon usage in bovine prolactin mRNA is nonrandom, but, similarly to rat and human prolactins, it does not exhibit the strong preference for G or C in codon third positions seen in bovine, rat, and human growth hormone mRNAs. The translational termination signal in bovine prolactin in UAA, also the same as in rat and human prolactins and differing from the UAG "stop" codon used in bovine, rat, and human growth hormones and human chorionic somatomammotropin. The amino acid and mRNA nucleotide sequences of bovine, rat, and human prolactins and growth hormones were compared by several techniques based on various theories of molecular evolution. The comparison of prolactin to growth hormone is consistent in all three species, suggesting that the genes for these two hormones diverged about 350 million years ago. However, comparisons among the three prolactins or among the three growth hormones to determine the times of evolutionary divergence of the three species generated values that were inconsistent with each other and with the fossil record. Analysis of these discrepancies suggests that the genes for prolactin and growth hormone may now be evolving by different mechanisms.

Amino Acid Sequence↗

PubMed1993

The effect of nalmefene on pulsatile secretion of luteinizing hormone and prolactin in men.

Luteinizing hormone (LH) and prolactin are released in pulses which are relatively synchronous in the luteal phase of the menstrual cycle in women. The concordance of LH and prolactin pulses in normal men has not been reported. The objectives of this study were firstly to determine whether LH and prolactin pulses are synchronous in men, and secondly to examine the effects of naloxone and a new orally active opiate antagonist, nalmefene, on LH and prolactin release in men. Three groups of normal male subjects received saline infusion (control n = 5), naloxone infusion (2 mg/h; n = 5) or nalmefene (10 mg p.o.; n = 6). Blood samples were collected every 15 min for 2 h before and 6 h after study medication for determination of LH, prolactin and testosterone by radioimmunoassay. Both naloxone and nalmefene resulted in a significant increase in LH pulse frequency and in mean serum LH and testosterone concentrations with no change in LH pulse amplitude, prolactin pulse frequency or amplitude. In controls, 61% of LH pulses were synchronous with prolactin pulses. There was a decrease in concomitance of LH and prolactin pulses with naloxone (48%) and nalmefene (24%; P < 0.025) administration. In contrast, 52% of prolactin pulses were concomitant with LH pulses in controls, while naloxone (100%) but not nalmefene (67%) resulted in a significant (P < 0.01) increase in pulse synchrony. The difference observed between naloxone and nalmefene on prolactin--LH pulse synchrony is probably due to differential opioid receptor activity at the pituitary and hypothalamic level.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2004

Raised serum prolactin in rheumatoid arthritis: genuine or laboratory artefact?

OBJECTIVES: Serum prolactin concentrations have been reported as higher, similar or lower in patients with rheumatoid arthritis (RA) compared with control subjects. We investigated whether low biological activity macroprolactin (a prolactin antibody complex), which is detected variably in different prolactin immunoassays, could account for the discrepant total prolactin results reported in RA. METHODS: We compared serum total prolactin and free prolactin in 60 women with RA and 31 female controls. RESULTS: No subject had hyperprolactinaemia or macroprolactinaemia. Serum concentrations of total and free (monomeric) prolactin were higher (P<0.05) in women with RA [mean (s.d.), 225.6 (104.6) and 201.6 (95.4) mU/l respectively] compared with controls [175.0 (68.5) and 154.0 (60.9) mU/l respectively]. CONCLUSIONS: We report higher serum free prolactin concentrations in women with RA compared with control subjects. This result indicates that the higher serum total prolactin levels in patients with RA are the consequence of increased free prolactin concentrations and are not due to macroprolactin.

Arthritis, Rheumatoid↗

PubMed1998

Amniotic fluid prolactin is decreased by experimental intrauterine infection or interleukin-1beta infusion but not via prostaglandins in pregnant rhesus macaques.

Amniotic fluid contains a high concentration of prolactin produced and secreted by the decidua. In vitro models have suggested that bacterial products inhibit prolactin secretion by decidual cells. To further examine this potentially important regulatory mechanism in the whole animal, chronically instrumented pregnant rhesus monkeys were prepared. Experimental infection was induced by intraamniotic or choriodecidual inoculation of 10(3)-10(6) group B streptococcus. Alternatively, interleukin (IL)-1beta was infused into the amniotic cavity. Finally, indomethacin was coadministered with IL-1beta to block the production of prostaglandins (PGs). The average prolactin level prior to inoculation (0 h) equaled 34.0 +/- 6.4 microg/ml. There was a 40% decrease in prolactin by 37 h postinfection (n = 6) and a 71% decrease between 61 and 72 h postinfection (n = 3, p < 0.01 vs. before infection). Infusion of IL-1beta also caused a decrease in amniotic fluid prolactin. There was a 42% decrease in prolactin between 0 and 24 h postinfusion (p < 0.05) and a 66% decrease between 25 and 72 h after IL-1beta infusion (p < 0.05; n = 6). Coadministration of indomethacin with IL-1beta prevented the accompanying increase in PGs but did not prevent the decrease in prolactin (n = 5). Amniotic fluid prolactin levels in untreated monkeys were stable and without a prepartum decline during the sampling period from 130 to 166 days of gestation. In summary, intrauterine bacterial infection decreases amniotic fluid prolactin, and IL-1beta mimics this effect. The effect of IL-1beta on amniotic fluid prolactin does not appear to be mediated by PGs and may involve a direct effect of IL-1beta on decidual cells.

Amnion↗

PubMed2002

Ethanol induces hyperprolactinemia by increasing prolactin release and lactotrope growth in female rats.

BACKGROUND: Alcohol drinking is known to cause hyperprolactinemia in both humans and laboratory animals. The mechanism by which alcoholism causes hyperprolactinemia is not known. This study investigated whether increased pituitary production of prolactin, which leads to alcohol-induced hyperprolactinemia, results from an increase in cell number and/or cell production of prolactin in the pituitary. METHODS: The effects of ethanol on lactotropes were determined in vivo using female rats as an animal model and in vitro using primary cultures of mixed rat anterior pituitary cells and enriched lactotropes. In vivo experiments involved administration of ethanol for 2 and 4 weeks using a liquid diet containing 8.7% ethanol (v/v), which provides 37% of the calories in cyclic, ovariectomized, and estradiol-17beta-treated ovariectomized Fischer-344 rats. The control group was pair-fed an isocaloric diet minus the ethanol or fed a normal diet ad libitum. These animals were used to determine ethanol's effects on plasma prolactin levels, pituitary wet weights, pituitary total protein levels, and the number of mitotic lactotropes. In vitro studies determined ethanol's effects in the presence and absence of estradiol on prolactin release and lactotropic cell proliferation. Prolactin levels in plasma and media samples were measured using radioimmunoassay. Mitotic lactotropes were determined using bromodeoxyuridine incorporation assay. RESULTS: Ethanol treatment increased in a time-dependent manner the plasma levels of prolactin in cyclic, ovariectomized, and estradiol-treated ovariectomized rats. Ethanol treatment also increased pituitary wet weight and/or pituitary total protein levels and DNA synthesis in lactotropes. Determination of ethanol's action on lactotropic cell proliferation and hormone secretion in vitro using primary cultures of mixed pituitary cells revealed that ethanol stimulated both basal and estradiol-induced prolactin secretion and lactotropic cell proliferation. When ethanol's actions were studied in isolated lactotropes, ethanol alone or in combination with estradiol stimulated prolactin secretion but failed to increase lactotropic cell proliferation. CONCLUSIONS: These results suggest that ethanol causes hyperprolactinemia by elevating prolactin release from lactotropes and by increasing the number of lactotropes in the anterior pituitary gland. The mitotic action of ethanol requires cell-cell communication between lactotropes and other pituitary cells. Furthermore, ethanol's mode of action on prolactin release and lactotrope growth is similar to that observed for estradiol.

Animals↗

PubMed2006

The relationship between prolactin levels and glucose homeostasis in antipsychotic-treated schizophrenic patients.

OBJECTIVES: To determine if prolactin levels are associated with glucose-insulin homeostasis in antipsychotic-treated patients with schizophrenia. METHOD: Prolactin levels and glucose homeostasis (quantified using oral glucose tolerance testing, insulin measurement, and homeostasis model assessment) were measured in 15 patients with elevated prolactin levels secondary to antipsychotic treatment of schizophrenia (mean age, 30.4 years; SD, 5.3 years). The effect of reducing prolactin levels by switching patients' antipsychotic treatment to clozapine was ascertained by performing the measures before and after the switch to clozapine. RESULTS: There was no significant correlation between prolactin and glucose-insulin measures at baseline. There was a large reduction in prolactin (593 mIU/L) after switching to clozapine, but this was not associated with changes in glucose-insulin measures. CONCLUSIONS: Prolactin is not a significant determinant of glucose-insulin homeostasis in patients taking antipsychotics for schizophrenia. There was no benefit from lowering prolactin levels using clozapine. This could be because prolactin does not have a major effect on glucose homeostasis or that the effects of prolactin reduction are countered by clozapine.

Adult↗

PubMed1976

Dissociation between TSH and prolactin dynamics in treated thyrotoxicosis.

TSH and prolactin secretory patterns in thyroid disease have generally been reported as concordant. We studied TSH and prolactin responses to TRH infusion (500 mug) in euthyroid individuals previously treated for thyrotoxicosis with 131I or antithyroid drugs. The 131I-treated group (seven men, twenty women) had been clinically and biochemically euthyroid (normal serum thyroxine and triiodothyronine levels) for 6 months to 4-5 years (kappa +/- SD = 17-1 +/- 4-1 months). Based on maximal TSH increment (deltaTSH), three patient groups were identified: Group 1 [normal deltaTSH, n = 6]: delta prolactin was normal in two, blunted in one and exaggerated in three. Group 2 (exaggerated TSH response, n = 8): delta prolactin was normal in two, blunted in one and exaggerated in five. Group 3 (TSH nonresponders, n = 13): delta prolactin was normal in five, blunted in three, and exaggerated in five. Eleven patients (three men, eight women) were studied after 6 months antithyroid-drug treatment. All were clinically and biochemically euthyroid. All but one showed a blunted TRH-TSH response. All three men showed an exaggerated delta prolactin as did four of eight women. Three women showed a blunted delta prolactin and in one, delta prolactin was normal. Thus, TRH-induced TSH and prolactin response patterns in treated thyrotoxicosis are not uniformly concordant, and, while a blunted or absent TSH response commonly persists long after euthyroidism has been restored, this is most frequently accompanied by a normal or exaggerated prolactin response.

Adult↗

PubMed1977

Effect of psychosocial stimuli and limbic lesions on prolactin at rest and following stress.

Many of the factors altering corticosterone in the rat have similar effects on prolactin. Resting prolactin, like corticosterone, is higher in animals housed singly than in those multiply housed. Unlike corticosterone, gentling did not lower prolactin. An exquisite sensitivity to environmental stimuli which results in rapid elevations in prolactin levels has been indentified in the rat which is considerably greater than that for corticosterone. Like corticosterone, the pattern of prolactin stress responses varies according to time of day. This differential sensitivity may well account for the diurnal variation in prolactin reported by some investigators. The limbic system has an important influence on prolactin. Lesions of the septal region do not modify resting levels but alter the pattern of prolactin stress responses in ways which are only partly similar to the effects of such lesions on corticosterone. In rhesus monkeys, individual variation in resting prolactin levels was observed, similar to that seen in the human. Levels are stable over periods of up to 50 days and are characteristic of the individual animal. In response to the stress of electric shock or shaping to a bar press response, prolactin elevation occurs only in animals with high resting levels, suggesting that a common mechanism is responsible for controlling both resting levels and magnitude of stress responses.

Animals↗

PubMed1981

The dynamics of prolactin secretion during the puerperium in women.

This study deals with serum prolactin concentrations during various conditions in the early puerperium in an attempt to investigate some characteristics of the mechanisms responsible for the regulation of the lactotropes. In nursing, in non-nursing, non-medicated and in non-nursing, bromocriptine-treated women prolactin and 17 beta-oestradiol were measured during the early puerperium. In the first and the third group this was repeated during and after challenge with oestradiol-benzoate. The pituitary responsiveness to TRH was also determined in these two groups, challenged and unchallenged with oestradiol-benzoate. Nursing women had higher prolactin levels than the non-nursing groups, while bromocriptine decreased prolactin to very low levels. Non-nursing non-medicated women had prolactin values between those of nursing and those of bromocriptine-treated mothers. The already elevated prolactin levels in nursing women were not influenced by chronic oestradiol administration. In non-nursing puerperal women treated with bromocriptine, exogenous oestradiol caused a significant rise in plasma prolactin. The prolactin response to TRH in nursing women was clearly reduced in comparison with the normal menstrual cycle. In the bromocriptine-treated group the basal concentration of prolactin and its response to TRH stimulation was similar to normal non-pregnant women. In nursing and in non-nursing women treated with bromocriptine prolactin responses to TRH were increased after oestradiol challenge.

Bromocriptine↗

PubMed1983

Inhibition of prolactin secretion by low-dose dopamine infusion in patients with hyperprolactinaemia.

Dopamine inhibits the secretion of prolactin from the pituitary. We have examined the relation between plasma dopamine and serum prolactin in 12 patients with hyperprolactinaemia during the infusion of dopamine at low doses (0.01, 0.1 and 1 microgram/kg/min). Plasma dopamine levels were raised from less than 100 pg/ml at the lowest rate of infusion to more than 20 000 pg/ml at the highest. Suppression of prolactin secretion was seen in some patients even at the lowest rate of infusion (0.01 microgram/kg/min); marked suppression of prolactin secretion (60%; 17--83%) was found at the intermediate dose (0.1 microgram/kg/min) in 11 of the 12 subjects with little further decrease in serum prolactin (70%; 50--87%) in those in whom the rate of dopamine infusion was increased ten-fold. One patient with the highest serum prolactin (82 500 mu/l) showed no decrease in prolactin either at the lowest or intermediate rates of dopamine infusion. Serum prolactin levels returned to values similar to or greater than basal on cessation of dopamine infusion. Infusion of dopamine at doses much lower than previously used in man exposes the pituitary to a concentration of dopamine sufficient to suppress prolactin secretion. These observations have important implications in understanding the pathophysiology of prolactin secretion from the pituitary gland and for future investigations of the control of hormone release by dopamine.

Depression, Chemical↗