Prolactin In Man Research Articles

Prolactin in Clinical Practice

ISOLATION of human prolactin and the development of highly sensitive and specific radioimmunoassays have allowed precise quantitation of serum prolactin concentrations in humans. Although changes in prolactin secretion have been described in a variety of physiologic and pathologic conditions, our understanding of the physiologic effects of prolactin is scant. Only the obligatory role of prolactin in lactation has been established. Since random serum prolactin concentrations are only slightly lower in normal men than in normal women, prolactin may have physiologic effects unrelated to lactation. The kidney¹and the adrenal²have been suggested as target organs for prolactin action. Further investigative efforts are required to explore the implications of these and other possible physiologic effects of prolactin in man. <h3>Regulation of Prolactin Secretion</h3><h3>Prolactin-Inhibitory Factor (PIF).—</h3> Prolactin secretion is primarily under tonic hypothalamic inhibitory control (Figure). Although a specific PIF has yet to be isolated, the importance of this

Osmotic control of prolactin release and its effect on renal water excretion in man

Prolactin appears to play a role in osmoregulation of fishes and birds and a possible contribution of this hormone to the regulation of salt and water excretion in mammals has been suggested as well. The present studies were undertaken to investigate the role of osmotic pressure on the secretion of prolactin and the effect of the hormone on renal water excretion in man. The i.v. administration of synthetic thyrotropin releasing hormone (TRH) (7 mug/kg) to five subjects undergoing a maximal sustained water diuresis increased serum prolactin to supraphysiologic levels in all as mean concentration rose from 30.2 +/- 2.9 to 60.2 +/- 5.0 ng/ml (P less than 0.005). This increase was not associated with either significant alterations in renal hemodynamics or sodium excretion and water excretion. The osmoregulation of prolactin release was then investigated by the oral administration of 20 ml/kg of water to seven subjects in 11 studies. While the water load decreased serum osmolality from 293 +/- 285 +/- 1.5 mOsm/kg H2O (P less than 0.001), there was no significant change in prolactin level, 28+/- 1.8 to 30 +/- 2.4 ng/ml. Serum hypertonicity was achieved in six subjects with the infusion of 5% NaCl which increased serum osmolality from 287 +/- 1.8 to 298 +/- 1.4 mOsm/kg (P less than 0.001). While the hypertonic state caused a marked antidiuresis as urinary osmolality rose from 62 +/- 5.9 to 480 +/- 48 mOsm/kg (P less than 0.001), the concentration of prolactin remained unchanged at 28 ng/ml. We conclude that supraphysiologic levels of prolactin have no antidiuretic properties in a vasopressin-free state and that acute alterations in serum tonicity within the range observed do not affect the release of prolactin in man.

Acute and Chronic Estrogen Effects upon Serum Somatomedin Activity, Growth Hormone, and Prolactin in Man

Estrogen (E) reduces bioassayable GH-dependent serum somatomedin (SM) activity in acromegalics without affecting plasma growth hormone (GH) levels and inhibits the rise of SM activity normally produced by GH administration in GH-deficient subjects. We have now investigated the effect of E administration on serum SM activity and on plasma GH and prolactin (PRL) in 6 adult male subjects without pituitary pathology. Chronic E administration (ethinyl estradiol 0.5 mg/day for 7 to 70 days) reduced serum SM activity by 40 to 62% in each of 4 subjects (P less than 0.02 to less than 0.001). In 3 of the subjects, basal GH levels increased by 75 to 300% (P less than 0.05 to less than 0.001) and basal PRL levels increased by 90 to 200% (P less than 0.01 to less than 0.001). While iv administration of normal saline did not significantly affect either SM or GH, iv administration of E (bolus injection of 25 mg conjugated estrogens, USP) to 5 subjects resulted in: a) a 46 to 80% decrease in serum SM activity in all subjects, proceeding with an apparent half-life of 2 hours, becoming significant (P less than 0.05) at 2 hours (1 subject) to 3 hours (4 subjects), maximal at 6 hours, and persisting for 12 to 24 hours; b) GH elevation to 3 to 16 times baseline level (P less than 0.01) at 2 to 3 hours in 4 subjects; and c) no significant change of PRL levels in any subject. The mean GH response to iv E was maximal at a time (2 hours) when the mean SM activity had decreased only 20% and subsided well before the nadir of SM activity. The one patient without GH response to chronic or acute E administration may have been affected by absorption of triamcinolone being applied topically during the study. These results demonstrate that in males with normal pituitary function, E reduces serum SM activity, enhances basal GH and PRL secretion, and, upon iv injection, stimulates acute GH release. Although opposite chronic E effects upon GH and SM activity support a putative negative SM-GH feed-back mechanism, iv E administration apparently provokes acute GH release by a different mechanism. The half-life of serum SM activity in the human is probably much shorter than previously estimated.

The effect of apomorphine on basal and TRH stimulated release of thyrotrophin and prolactin in man.

Studies were performed in two groups of healthy male volunteers to evaluate the effect of apomorphine on the secretion of thyrotrophin (TSH) and prolactin under basal conditions and following the administration of thyrotrophin releasing hormone (TRH). Apomorphine HCl, administered sc in a dose of 0.75 mg had no effect on the basal levels of plasma TSH or serum prolactin. The iv injection of 200 mug TRH was followed by an increase in TSH and prolactin in all subjects, with a maximum 20-30 min after the injection. When 0.75 mg of apomorphine was injected sc 30 min before TRH, the increase in prolactin was significantly reduced whereas the TSH response was unaltered. Our studies indicate that the TRH induced secretion of prolactin in man can be suppressed through a dopaminergic mechanism whereas the secretion of TSH is not influenced.

The effect of chlorpromazine on the secretion of immunoreactive beta-MSH and prolactin in man.

The effect of chlorpromazine (50 mg. im) on the plasma concentration of immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) and prolactin was studied in 8 hospitalized subjects with non-endocrine skin disorders. Plasma beta-MSH concentrations remained unchanged over a period of 7 h in 6 subjects. In the remaining 2 subjects there was a slight increase. Plasma prolactin concentrations were greatly increased in all subjects 1 1/2-3 h after the injection and had almost returned to pre-injection levels by 7 h. This suggests that the control of beta-MSH secretion in man, unlike that of prolactin in man and MSH peptides in other mammals, is not predominantly inhibitory. The reason for this discrepancy may be that beta-MSH is not a natural MSH in man and occurs as part of the lipotropic hormone (LPH) or as a breakdown product.

Failure of oral water loading and intravenous hypotonic saline to suppress plasma prolactin in man.

To test the effect of acute changes in plasma osmolality on plasma prolactin concentrations, the hormone was measured before and during oral water loading, hypotonic saline infusion, and hypertonic saline infusion in normal subjects. In 10 normal men there was a small but statistically significant rise in mean prolactin, from 7.6 to 12.3 ng/ml, occurring within half an hour after the ingestion of a water load of 20 ml/kg. A small but statistically insignificant rise in mean plasma prolactin was observed in 11 normal women, although there was a significant negative correlation between plasma prolactin and plasma osmolality in these subjects. No effect of the intravenous infusion of either hypotonic saline (0.45%) or hypertonic saline (5%) on mean plasma prolactin was noted in 5 normal men. These studies do not confirm a previously reported suppression of prolactin concentrations by oral water loading of hypotonic saline infusions in normal subjects. While the data suggest a negative correlation between plasma osmolality and plasma prolactin, at least after water loading, they do not support a physiological role for prolactin in the short-term regulation of plasma osmolality in humans.

Prolactin release in cattle.

The cow has been specifically selected for lactational performance. It has no lactational anoestrus and the simultaneous reproductive ability and milk yield have not only scientific interest but economic importance too. We have no evidence of a luteotrophic action of prolactin (Hoffmann, Schams, Bopp, Ender, Gim\l=e'\nez& Karg, 1974) in this species such as has been shown in some others. Furthermore, mammary cancer, one motivation for the increasing amount of work devoted to studies on prolactin in man, has not been recorded in the cow.

Editorial: Control of prolactin in man.

The isolation of human growth hormone, an important event of nearly 20 years ago, was followed by the observation that unusual lactogenic activity resided in this polypeptide. As a result the notio...

THYROID HORMONE INHIBITION OF THE PROLACTIN RESPONSE TO THYROTROPIN—RELEASING HORMONE

Abstract The influence of serum triiodothyronine (T3) and thyroxine (T4) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Δ prolactin) was used as the index of response to TRH. In 12 patients with primary hypothyroidism, the maximum Δ prolactin in response to TRH fell from 100.5±29.1 ng/ml (mean ±SEM) before treatment to 36.1±6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 μg T3 + 120 μg T4 daily. The mean serum T3 level increased from 57±8 to 138±10 ng/100 ml, and the mean serum T4 level increased from 3.0±0.4 to 7.2±0.4 μg/100 ml during this treatment. In eight normal subjects the maximum Δprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 μg T3 + 120 μg T4 daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Δprolactin in response to TRH increased from 14.2±2.9 ng/ml before treatment to 46.9±6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T3 level fell from 313±47 to 90±8 ng/100 ml, and the mean serum T4 level fell from 20.8±2.5 to 6.8±0.6 μg/100 ml during this treatment. These results show that changes from normal serum levels of T3 and T4 are associated with changes in prolactin responses to TRH; subnormal serum levels of T3 and T4 increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T3 and T4 inhibit this release.

Thyroid hormone inhibition of the prolactin response to thyrotropin-releasing hormone.

The influence of serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations on the release of prolactin in man was studied by determining the prolactin response to synthetic thyrotropin-releasing hormone (TRH) in hypothyroid and hyperthyroid patients before and after correction of their serum thyroid hormone abnormalities. The maximum increment in serum prolactin above the basal level (maximum Delta prolactin) was used as the index of response to TRH. In 12 patients with primary hypothyroidism, the maximum Delta prolactin in response to TRH fell from 100.5+/-29.1 ng/ml (mean +/-SEM) before treatment to 36.1+/-6.0 ng/ml (P < 0.01) during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily. The mean serum T(3) level increased from 57+/-8 to 138+/-10 ng/100 ml, and the mean serum T(4) level increased from 3.0+/-0.4 to 7.2+/-0.4 mug/100 ml during this treatment. In eight normal subjects the maximum Deltaprolactin in response to TRH was not significantly different during the 4th wk of treatment with 30 mug T(3) + 120 mug T(4) daily from the response before treatment. In 10 patients with hyperthyroidism, the maximum Deltaprolactin in response to TRH increased from 14.2+/-2.9 ng/ml before treatment to 46.9+/-6.7 ng/ml (P < 0.001) during antithyroid treatment. The mean serum T(3) level fell from 313+/-47 to 90+/-8 ng/100 ml, and the mean serum T(4) level fell from 20.8+/-2.5 to 6.8+/-0.6 mug/100 ml during this treatment. These results show that changes from normal serum levels of T(3) and T(4) are associated with changes in prolactin responses to TRH; subnormal serum levels of T(3) and T(4) increase TRH-induced prolactin release, whereas substantially higher than normal serum levels of T(3) and T(4) inhibit this release.

Prolactin and thyrotropin release in man by synthetic pyroglutamyl-histidyl-prolinamide

Synthetic pyroglutamyl-histidyl-prolinamide or thyrotropin-releasing-hormone (TRH) stimulates secretion of prolactin (PRL) as well as thyrotropin (TSH) but has no consistent effect on serum levels of growth hormone (GH), luteinizing hormone (LH) or follicle stimulating hormone (FSH) in man. After intravenous injection of as little as 10 μg TRH, both serum PRL and TSH levels rise rapidly. The PRL and TSH response was greater in normal women than in normal men and both responses were greatly enhanced in hypothyroid patients and virtually abolished in hyperthyroid patients. The possibility that p-Glu-His-Pro-NH 2 is also a “natural physiological” regulator of PRL in man is evident.

Some Metabolic Effects of Ovine Prolactin in Man

Some Metabolic Effects of Ovine Prolactin in Man