Normal Prolactin Responses Research Articles

A Catecholamine Precursor Does Not Influence Exercise Performance in Warm Conditions.

Acute doses of Sinemet® (L-DOPA combined with carbidopa) previously failed to influence prolonged exercise performance in a temperate environment, but it is not known whether acute doses of L-DOPA timed to reach maximum plasma concentrations (Cmax) during exercise will improve prolonged cycling performance in warm conditions (30.2°C ± 0.2°C, 50% ± 1%). Ten physically active men (age, 26 ± 4 yr; height, 1.76 ± 0.08 m; body mass, 76.3 ± 10.6 kg; V˙O2peak, 57 ± 8 mL·kg(-1)·min(-1)) were recruited for this study. Participants cycled for 1 h at 60% V˙O2peak followed by a 30-min exercise test, during which they were instructed to complete as much work as possible. Heart rate, skin and core temperatures, as well as RPE and thermal stress were recorded throughout the exercise, and blood samples were collected at rest, at 15-min intervals during the first hour of exercise, and at the end of the exercise test. Finger tapping tests at the beginning and end of the exercise were conducted to examine fine motor control. There was no significant difference in the work done on the placebo (314 ± 43 kJ) and L-DOPA trials (326 ± 48 kJ, P = 0.276). Prolactin concentrations were increased at the end of the exercise in all trials (P < 0.001), but this response was attenuated at the end of the exercise for the L-DOPA trial (11.4 ± 5.5 ng·mL(-1)) and placebo trials (20.8 ± 3.3 ng·mL(-1), P = 0.003). No differences between trials were found for any other measure. The results suggest that increasing central catecholamine availability inhibits the normal prolactin response to exercise in the heat but does not alter performance, thermoregulation, or sympathetic outflow.

Prolactin Secretion in Myotonic Dystrophy

In order to evaluate prolactin secretion in females with myotonic dystrophy (MD) prolactin responses to TRH, metoclopramide and bromocriptine were studied in 13 women with myotonic dystrophy (10 normoprolactinaemic and 3 hyperprolactinaemic) and 8 healthy women. Following TRH administration mean maximal net increase was significantly higher in a group of normoprolactinaemic patients with MD in comparison to controls (p less than 0.05). In three patients with increased basal prolactin levels an exaggerated prolactin response to TRH has been observed. Normal prolactin response in a group of normoprolactinaemic as well as in hyperprolactinaemic patients have been observed following metoclopramide bolus injection. Following bromocriptine administration, maximal net decrease in prolactin levels has been found to be greater in normoprolactinaemic patients compared to healthy subjects, although the difference was statistically insignificant. The suppressive action of bromocriptine was more pronounced in patients with hyperprolactinaemia. Those results showed that there is some derangement in prolactin secretion in myotonic dystrophy leading to increased prolactin levels in some patients. Although the mechanism of this derangement has not been clarified yet it seems that it is not mediated via dopaminergic receptors.

Testicular function and prolactin responsiveness to TRH and cimetidine after renal transplantation.

The hypothalamic-pituitary-testicular axis and the regulation of prolactin secretion were investigated in eleven male renal transplant recipients. Mean serum levels of testosterone and estrone were normal, whereas those of androstenedione and estradiol were low. Mean basal luteinizing hormone (LH) levels were slightly elevated, but the peak responses to 50 micrograms i.v. gonadotropin-releasing hormone (GnRH) were not dissimilar from controls. Both basal and GnRH-stimulated follicle-stimulating hormone (FSH) levels were elevated (p less than 0.02-0.05) and also positively correlated with the time spent on hemodialysis (p less than 0.005-0.002). Basal prolactin (PRL) levels were normal, in all subjects. Nine out of 11 patients had a normal PRL response to Thyrotropin-releasing Hormone (TRH). However only six out of 11 had a normal response to 200 mg i.v. Cimetidine (Cim). Three subjects normally responding to TRH failed to respond to Cim. Uremic primary hypogonadism is not fully reversed by renal transplantation: a slight defect in the pituitary LH release may persist and the impairment of the tubular testicular function is left unchanged. While uremic hyperprolactinemia is corrected, the responsiveness to PRL-stimulating agents, particularly Cim, is not restored to normal, reflecting a derangement at the pituitary as well as the hypothalamic level.

Dose-response studies with thyrotropin-releasing hormone: evidence for differential pituitary responses in men with major depression, alcoholism, or no psychopathology.

A reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) has been reported in both alcoholic and depressed men. To discern whether the pathophysiological basis of a reduced TSH response is similar in these two disorders, the present study compares the dose-response patterns of TSH and prolactin (PRL) to TRH in depressed, alcoholic, and control men. Four doses of TRH (25, 100, 500, and 800 micrograms) were given at several day intervals to 6 men with major depression, 8 men with alcohol dependence, and 7 control men. Examination of the pattern of TRH-induced TSH and PRL response revealed differences for each paired group comparison: depressed versus control, depressed versus alcoholic, and alcoholic versus control. Compared with controls, depressed men had low TSH and low PRL responses to TRH, whereas alcoholic men had low TSH responses and normal PRL responses. Levels of neither thyroid hormones, cortisol, or sex steroids, nor age or body size, explained these differences. These findings suggest that the pathophysiological basis of a reduced TSH response to TRH is different in alcoholism, compared with depression.

Tachykinins induce secretion of prolactin from perifused rat anterior pituitary cells by interactions with two different binding sites.

Substance P and the two other mammalian tachykinins, neurokinin A and B, are accepted to have direct regulating effects at the anterior pituitary level. We have examined the effects of substance P (SP) and neurokinin B (NKB), alone and in combination, on prolactin release from cultured anterior pituitary cells grown on collagen-coated micro beads and placed in a perfusion system. Prolactin (Prl) secretion was observed within 25 s after exposure to either secretagogue and reached a maximum within 60-80 s. Furthermore, the prolactin response induced by SP and NKB was dose-dependent. Prl secretion remained constant for up to 4 h when SP or NKB were perifused and then fell gradually towards basal levels. Simultaneous addition of submaximal concentrations of SP and NKB resulted in an additive response compared with the responses of either secretagogue alone. Continuous (8 h) perifusion with SP did not prevent a normal prolactin response by NKB or TRH. These results indicate that the tachykinins, substance P and neurokinin B, release Prl from perifused female rat anterior pituitary cells by interaction with two different receptors, possibly the NK1 and NK3 tachykinin receptor subtypes.

Prolactin responses to phenylalanine and tyrosine in phenylketonuria

In normal subjects, ingestion of tyrosine or phenylalanine stimulates prolactin (PRL) secretion. In patients with phenylketonuria (PKU), we found normal PRL responses to phenylalanine, demonstrating that conversion of phenylalanine to tyrosine is not necessary for PRL stimulation. PKU patients also showed greater PRL responses to tyrosine during dietary phenylalanine restriction than when consuming an unrestricted diet; this finding is consistent with inhibition by phenylalanine of tyrosine transport across the blood-brain barrier. Such competitive inhibition of a normal brain function may serve as a model for some of the neurotoxic effects of phenylalanine in PKU.

Hyperresponsiveness of TSH and prolactin and impaired responsiveness of GH in Japanese patients with isolated ACTH deficiency

Two hundred and forty-one cases of isolated ACTH deficiency have been reported in Japan since 1969. Pituitary hormone responsiveness to stimulation tests before and after hydrocortisone supplementation was investigated in these cases. Plasma ACTH level showed no or little change in response to lysine vasopressin, metyrapone, CRF or insulin-induced hypoglycemia in 97.3-100% of the cases. Serum GH level changed little or not at all in response to GRF, insulin-induced hypoglycemia, glucagon, 1-dopa and arginine in 26.9, 29.3, 40.0, 50.0 and 56.1%, respectively. Serum TSH and prolactin (PRL) levels showed hyperresponse to TRH in 34.7 and 35.6%, respectively. After hydrocortisone therapy, GH secretion was more responsive than before therapy in 78.9% of the cases. After supplementation, TSH level was less responsive to TRH stimulation than before therapy in 59.3% of the cases. After hydrocortisone supplementation, TSH response to TRH decreased in 75% of ACTH-deficient patients without primary hypothyroidism but did not decrease in more than half of those with primary hypothyroidism. TSH response to TRH decreased after supplementation in 76.5% of the patients with TSH hyperresponsiveness before therapy, and increased after therapy in 66.7% of those with normal TSH responses before therapy. After supplementation, PRL response to TRH was less than that before therapy in 43.5% of ACTH--deficient patients, and greater than that before therapy in 30.4%. PRL response to TRH decreased after therapy in 66.7% of the patients with PRL hyperresponsiveness before therapy, and increased in 63.6% of those with normal PRL response before therapy. Primary hypothyroidism and Hashimoto's thyroiditis were complicated in 21.6 and 11.6%, respectively, of the 241 patients with isolated ACTH deficiency. In patients who had TSH hyperresponsiveness and/or high basal TSH levels and PRL hyperresponsiveness and/or high basal PRL levels, primary hypothyroidism was complicated in 58.4 and 42.3%, respectively. Hashimoto's thyroiditis was complicated in 29.8 and 20.5%, respectively, of these patients. Pituitary cell antibody (PCA) was detected in 36.6% of ACTH-deficient patients who were examined. Pituitary cell surface antibody (PCSA) to AtT-20 cells and GH3 cells was detected in 50.0 and 28.0% of the examined cases, respectively. The prevalence of PCA and PCSA did not differ between TSH-hyperresponsive patients and those with normal TSH basal levels and response, whereas PCA and PCSA were significantly more prevalent in PRL-hyperresponsive patients than in those with normal PRL levels and response. An empty sella was found in 30.2% of the examined case.(ABSTRACT TRUNCATED AT 400 WORDS)

Role of calcium in dopaminergic regulation of TRH- and angiotensin II-stimulated prolactin release

The contributions of intracellular and extracellular calcium to thyrotropin-releasing hormone (TRH)- and angiotensin II (ANG II)-stimulated prolactin (PRL) release and the role of calcium in dopaminergic inhibition of these events were examined because of unresolved controversies in these areas. Dispersed normal female rat anterior pituitary cells were used to evaluate radiocalcium fluxes and the intracellular calcium concentration ([Ca]i). Both peptides increased PRL release, fractional 45Ca2+ efflux, and [Ca]i in a spike and plateau pattern, and neither increased 45Ca2+ uptake. In a low-calcium buffer, TRH and ANG II stimulated less than 5% of the normal PRL response, yet efflux was at least 50% of normal and [Ca]i was 20-40% of normal. Dopamine reduced TRH-stimulated PRL release by greater than 90% and abolished the plateau, yet the calcium responses to TRH were at least 50% of normal. Although dopamine prevented the plateau component of peptide-stimulated [Ca]i, the plateau phase of efflux persisted. Thus TRH and ANG II may control at least two cell-associated calcium pools, one readily depleted and the other highly resistant to depletion, without evidence for stimulation of calcium uptake. Dopamine inhibits PRL release stimulated by these peptides, with a relatively greater influence on the plateau component, through mechanisms only minimally related to calcium flux. Dopamine may slightly increase the extrusion of calcium mobilized by these peptides and thus may limit the anticipated increase in [Ca]i.

The effect of thyrotropin-releasing hormone stimulation on serum levels of gonadotropins in women during the follicular and luteal phases of the menstrual cycle

Thyrotropin-releasing hormone (TRH) can stimulate the secretion of adenohypophyseal thyroid-stimulating hormone and prolactin (PRL). The effect of TRH on gonadotropin secretion has not been well defined. This study investigated the effect of TRH administration on the peripheral levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) during the early follicular and midluteal phases of the menstrual cycle in five ovulatory, euthyroid, and normoprolactinemic women. Two hundred micrograms of TRH were administered intravenously on days 3 to 5 and on days 21 to 23 of the same cycle. LH and FSH were measured prior to and every 30 minutes for 2 hours following TRH injection. Ovulation was confirmed in all cycles by midluteal progesterone. All women had normal thyroid-stimulating hormone (TSH) and PRL responses to TRH stimulation in both cycle phases. Baseline and stimulated gonadotropin levels were analyzed by analysis of variance. Thirty minutes following TRH infusion, follicular and luteal levels of LH (mIU/ml, mean +/- standard error of the mean) significantly increased from 6.0 +/- 0.8 to 8.0 +/- 1.1 (P less than 0.005), and from 4.8 +/- 0.6 to 7.6 +/- 0.7 (P less than 0.005), respectively. Levels of FSH increased during both phases of the cycle, but the elevation was not statistically significant. These results suggest that TRH can stimulate gonadotrope secretion of LH, but not of FSH, in both the follicular and luteal phases of the cycle.

Thyrotropin-releasing hormone and gonadotropin-releasing hormone test to predict effectiveness of bromocriptine therapy in infertile women

Sixty-four infertile women presenting with luteal phase defect, anovulatory cycle, and secondary amenorrhea were compared with 15 normal cycling women with bolus injections of thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (GnRH) before bromocriptine (BCPT) therapy. All of the women had normal baseline prolactin (PRL), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) concentrations. Responses of PRL, LH, and FSH levels were measured. PRL responses in BCPT responders were markedly greater than in controls and nonresponders. A better responder rate to BCPT therapy was observed in patients with apparent (88.9%) or borderline (69.2%) exaggerated responses of PRL to TRH than in normal patients (41.7%). Further, in patients with normal PRL responses, the inappropriately enhanced LH responses were seen in BCPT responders but not in nonresponders. These findings suggest that TRH and GnRH tests are worthwhile in predicting the outcome of BCPT therapy in infertile patients.

Twenty-four-hour prolactin secretory patterns in women with galactorrhea, normal menses, normal random prolacting levels and abnormal sellar tomograms.

During a systematic study of women with idiopathic galactorrhea, we observed several patients with normal random serum prolactin (PRL) levels and normal menses, but abnormal sellar tomograms characteristic of a pituitary adenoma. To test the hypothesis that these women might have intermittent PRL hypersecretion, we studied PRL secretion by sampling blood every half hour for 24 h in 10 patients and for 17.5 h in another, and compared the findings to those of a group of 5 normal women. The mean 24-h PRL of the 10 patients (16.8 +/- 7.8 ng/ml; mean +/- SD) was not significantly different from that of the normal women (13.6 +/- 3.2 ng/ml), and each patient showed a normal sleep-associated PRL increment. Three individuals exhibited an abnormally elevated 24-h PRL (greater than 20 ng/ml). Increased PRL secretion occurred primarily at night or in the afternoon. Thyrotropin releasing hormone (TRH) administration caused normal or exaggerated PRL responses in all patients tested. High resolution CT scanning of two of the hypersecretors suggested a microadenoma in one case. In another case whose PRL was normal over 17.5 h, transsphenoidal surgery, carried out because of the tomographic findings and the symptom of headaches, demonstrated a 5-mm chromophobe adenoma that did not contain PRL by immunohistochemistry. Postoperatively the galactorrhea persisted. We conclude that most women with galactorrhea, normal PRL, normal menses, and abnormal tomograms have normal PRL secretion. However, a minority of patients with this syndrome do demonstrate intermittent PRL hypersecretion. The etiology of intermittent PRL hypersecretion and its relevance to galactorrhea have not been determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Nocturnal hypoxia and prolactin secretion in obese women.

Respiration during sleep was studied in six obese women who had impaired prolactin response to insulin induced hypoglycaemia (non-responders), six obese women with a normal prolactin response to hypoglycaemia (responders), and six lean women. Sleep apnoea did not occur in any subject. All the obese women showed a decrease in haemoglobin oxygen saturation when asleep, which occurred predominantly during periods of rapid eye movement sleep. That the fall in oxygen saturation was significantly greater (p less than 0.05) in the obese non-responders suggests that central as well as mechanical factors may be important for the genesis of nocturnal hypoxia and is evidence for a disturbance of central nervous function in some obese women.

Plasma prolactin response to thyrotropin releasing hormone in children with newly diagnosed insulin dependent diabetes.

The basal and TRH-induced prolactin (PRL) and TSH secretions were examined in 14 children aged 4 to 13 years with newly diagnosed insulin dependent diabetes (IDD) within three weeks after diagnosis. Basal PRL levels did not differ from the values of control. In response to TRH, 6 out of 14 patients showed an exaggerated PRL response and 8 a normal PRL response. The basal and TRH-induced TSH secretions were normal, while plasma triiodothyronine (T3) and thyroxine (T4) concentrations were significantly (p less than 0.001, p less than 0.02) lower in patients than in controls. These findings suggest that a significant proportion of children with newly diagnosed IDD has an exaggerated PRL response to TRH, and TSH secretion remains unchanged despite significant decreases of circulating thyroid hormone levels.

Gonadotrophin, testosterone and prolactin interrelationships in cadmium-treated rats.

We have investigated the long-term effect of a single subcutaneous injection of cadmium chloride on plasma testosterone and gonadotrophin levels and the prolactin response to the dopaminergic antagonist metoclopramide in the rat. Twelve days after treatment with cadmium there was testicular necrosis, associated with a decrease in testosterone concentration and atrophy of the accessory sexual glands. By 185 days, partial recovery of the accessory sexual glands indicated by Leydig cell regeneration and a slight rise in testosterone levels had occurred. There was, however, persistent damage to the germinal epithelium. Concentrations of LH increased eightfold above controls by day 12, remained raised until 60 days and then decreased to threefold above controls at 280 days. In contrast, FSH levels reached a maximum between 60 and 130 days and remained persistently raised. The peak prolactin response to metoclopramide in cadmium-treated rats was depressed 12 days after cadmium administration and levels remained low at 19 and 75 days. Normal prolactin responses to metoclopramide were obtained 130 days after cadmium treatment using 1:0 mg metoclopramide/kg or 280 days after treatment using 0.25 mg/kg. When control and cadmium-treated rats were castrated at 280 days and then given metoclopramide 10 days later, the prolactin response was significantly reduced. It is concluded that the impaired prolactin response to metoclopramide in cadmium-treated rats is reversible. Prolactin returns to normal in parallel with regeneration of the Leydig cells, partial restoration of the accessory sex organ weight, slight increase in plasma testosterone and decrease in LH levels. These results suggest that testosterone is not solely responsible for the maintenance of normal prolactin secretion in the male rat.

Abnormal regulation of prolactin secretion after successful surgery for prolactin-secreting pituitary tumours.

Patients with prolactin-secreting pituitary tumours have a diminished prolactin (PRL) response after administration of a variety of stimulatory agents, including thyrotrophin-releasing hormone (TRH), chlorpromazine (CPZ) and insulin-induced hypoglycaemia. We examined responses to these agents in sixty-seven women with PRL-secreting tumours before and after trans-sphenoidal surgery. Twenty-nine of the women were cured as defined by restoration of normal serum PRL concentrations and resumption of regular menses. One year following trans-sphenoidal surgery, patients with normal PRL concentrations and regular menses had normal PRL responses to TRH, while the responses to CPZ and insulin hypoglycaemia were not improved. The reversible impairment of PRL response to TRH reflects suppressed function of normal PRL-secreting cells, and the persistence of abnormal PRL responses to provocative stimuli after successful tumour removal may reflect some fundamental defect in the regulation of PRL secretion in patients with PRL-secreting adenomas. When growth hormone (GH) reserve after insulin hypoglycaemia was represented as the mean absolute increment above the basal concentration and compared with normal subjects, women with PRL-secreting tumours had a diminished response that returned to normal after successful surgery. This reversible impairment of GH secretion is not adequately reflected by standard criteria for GH response and suggests that PRL may have a role in the regulation of GH secretion.

ALTERED DOPAMINERGIC REGULATION OF THYROTROPHIN RELEASE IN PATIENTS WITH PROLACTINOMAS: COMPARISON WITH OTHER TESTS OF HYPOTHALAMIC‐PITUITARY FUNCTION

This study was carried out to test the hypothesis that sustained hyperprolactinaemia in patients with prolactinomas stimulates hypothalamic dopaminergic activity via a short loop positive feedback effect of prolactin (PRL). The intensity of dopamine (DA) effects on the pituitary around the adenoma was evaluated by measuring thyroid stimulating hormone (TSH) responses to intravenous injection of domperidone (10 mg) a new DA receptor blocking drug that does not penetrate the blood-brain barrier. TSH responses have been compared with those of PRL to the same agent. Eight females with prolactinomas showed greater TSH release after domperidone than nine normal females (sum of TSH increments over 20 min 17.5 +/- 1.7 v. 8.9 +/- 1.5 mu/l, P less than 0.001) whilst PRL release was reduced (sum of PRL increments over 120 min 5.9 +/- 2.4 v. 21.8 +/- 3.8 mu/l x 10(-3), P less than 0.01). Amongst nineteen hyperprolactinaemic females with apparently normal pituitary fossae (plain skull X-ray), ten showed an exaggerated TSH response (delta TSH, 4.2 +/- 0.6 mu/l, range 2.5-9.0 mu/1) and reduced PRL response to domperidone, comparable with established tumor cases. In the remaining nine normal fossa hyperprolactinaemic females, the TSH and PRL responses to dopaminergic were similar to normal females. These results support the initial hypothesis and indicate the coexistence of a defect in the dopaminergic inhibition of PRL release and increased dopaminergic inhibition of TSH release in patients with prolactinomas. The presence of an exaggerated TSH response to DA antagonism in a euthyroid, radiologically normal (plain skull X-ray), hyperprolactinaemic patient is compatible with the presence of an autonomously-functioning, PRL secreting, pituitary microadenoma and the TSH changes seen in these patients after DA antagonist administration can be readily detected by sensitive TSH radioimmunoassay.

The use of thyrotropin-releasing hormone in distinguishing prolactin-secreting pituitary adenoma

In order to differentiate between a prolactin-secreting adenoma and a nonneoplastic etiology for galactorrhea, a single stimulatory dose of 500 μg of thyrotropin-releasing hormone (TRH) was employed to assess the prolactin (PRL) response of 50 women. The results were compared to those obtained in 19 control subjects (10 with subsequent surgical removal of a PRL-secreting adenoma and nine women stimulated in the early follicular phase). All patients were grouped according to normal or elevated serum PRL, and normal, equivocal, or abnormal findings by tomography of the sella turcica. Patients with a normal baseline PRL had a normal PRL response to TRH of at least 200% above baseline. This normal response was independent of findings by tomography of the sella turcica. A highly significant difference in response (p < 0.001) was illustrated by all patients with elevated PRL and abnormal tomograms, and in some patients with elevated PRL and normal or equivocal tomograms. These responses were identical to those of the control patients who had histologic evidence of a PRL-secreting adenoma. The findings indicate that a PRL-secreting adenoma in patients with galactorrhea can be identified on the basis of the PRL response to TRH stimulation.

Prolactin response to exercise, metoclopramide and other provacative agents in children.

Metoclopramide (MCP), a derivative of procainamide was compared with exercise, arginine, insulin and thyrotropin releasing hormone (TRH) as a prolactin (PRL) releaser in children. The peak response of plasma PRL after oral administration of MCP was greater than that after strenuous exercise and after i.v. administration of pharmacodynamic agents. Normal PRL and TSH responses were observed after TRH administration in all subjects. Variable PRL responses were seen after exercise and after i.v. administration of arginine and insulin, despite significant growth hormone (GH) release following the administration of these agents. MCP produced no increase in plasma TSH. Metoclopramide may be useful for dynamic testing of PRL release in children. It can be taken orally and is free of side-effects.

The effect of metoclopramide, TRH and L-dopa on prolactin secretion in pituitary adenoma and in "functional" galactorrhoea syndrome.

The degree of autonomy in prolactin secreting pituitary adenomas and also prolactin secretory reserve in cases with suspected functional galactorrhea syndrome was evaluated with the use of metoclopramide, TRH and L-DOPA. It was found that in patients with pituitary adenoma the basal prolactin (PRL) level often exceeded 150 micrograms/l and the response to stimulation with TRH and/or metoclopramide was markedly diminished or even nonexistent, while the response to L-DOPA was usually retained. In patients with galactorrhoea and/or amenorrhoea, with normal skull X-ray the basal PRL level was either normal or moderately raised but the response to stimulation was various; mostly it was excessive, it was sometimes normal, but in some other cases it was markedly diminished as in patients with adenoma. In the author's opinion the so-called "functional disorder" of prolactin secretion is mainly hyperresponsiveness to stimulation, whereas the basal PRL level in those cases is usually normal or only intermittently raised. In the cases with a moderate hyperprolactinaemia, especially if it appears to be constant, and the response to stimulation is diminished or none at all, we suspect a pituitary microadenoma. Finally, there are rare cases of galactorrhoea with normal basal PRL and normal response to stimulation, in which the sensitivity of the mammary PRL receptor is probably increased. We suggest therefore that the above mentioned PRL stimulation tests may help in distinguishing between tumoural and functional hyperprolactinaemia.

Laboratory assessment of prolactin status.

The laboratory assessment of prolactin status was evaluated by detailed study of 921 subjects (587 normal subjects and 334 patients with pathological conditions). The effect on serum prolactin levels of age, sex, circadian rhythm, pulsatility of secretion, stress, drug ingestion, and pregnancy was defined in normal subjects. The normal prolactin responses to stimulation (TRH metoclopramide) and suppression (L-dopa, bromocriptine) were also determined. Basal prolactin levels were measured in patients with defined pathological conditions including prolactinoma, idiopathic hyperprolactinaemia, acromegaly, Cushing's disease, chronic renal failure, primary hypothyroidism, pituitary ablation, Kallman's syndrome, Nelson's syndrome, growth hormone deficiency, gonadotrophin deficiency, craniopharyngioma, panhypopituitarism, and chronic progressive arthropathy. Based on these data, a strategy for the routine laboratory assessment of prolactin status is outlined.