Circulating Concentrations Of Prolactin Research Articles

Physiological evidence for the existence of prolactin releasing factor: stress-induced prolactin secretion is not linked to dopaminergic receptors.

Experiments were undertaken to demonstrate the existence of a physiological role of prolactin releasing factor (PRF). Hypothalamic control of prolactin secretion is achieved by secretion of prolactin inhibiting factor (PIF) and/or PRF. Since the putative PIF is dopamine, complete blockage of the dopaminergic PIF receptors should permit demonstration of PRF activity. The changes in prolactin concentration were monitored by taking a blood sample every 2 min through an indwelling atrial cannula. An excessive amount of pimozide (3 mg/kg) was used to block dopaminergic receptors and prolactin concentration was elevated as a result. This higher concentration of circulating prolactin was maintained for more than 30 h after a bolus injection of pimozide. In this situation, lacking functional dopaminergic PIF receptors, there were fluctuations in the circulating prolactin concentration throughout the experiment. If, after pimozide administration, rats were exposed to an acute (ether) stress, the stress consistently elevated the circulating prolactin concentration. Since there are no functional dopaminergic PIF receptors available under these conditions, a dopaminergic PIF cannot be involved in producing the prolactin surge induced by the acute stress. Therefore, these results suggest that a physiological PRF is involved in the generation of this prolactin surge, through the evidence is not direct.

Serum prolactin and tumors of the prostate: unchanged basal levels and lack of correlation to serum testosterone.

To investigate the possible role of circulatory levels of prolactin on the development of prostatic tumors, and to gain insight into the prolactin-androgen relationship, serum prolactin and testosterone were determined in 73 patients with newly diagnosed prostatic adenocarcinoma. Controls consisted of 32 patients with benign prostatic hyperplasia before treatment, 19 age-matched controls, and 21 young individuals. Hormones were measured under standardized conditions by highly specific and sensitive radioimmunoassays. There was no difference in prolactin in the elderly men regardless of prostate pathology, but a significant increment was found in young controls. Individual prolactin values did not correlate with serum testosterone, and there was no statistical regression in prolactin values of patients in the age range between 50 and 80 years. In a second study, serum testosterone and prolactin were measured in 7 patients with prostate cancer and in 6 individuals with benign prostatic hyperplasia before and 30 and 60 minutes after stimulation with an iv bolus of 200 microgram TRH. Both hormones were within the normal range at time T0, and a significant stimulation of prolactin was achieved (p less than 0.001). Prolactin values did not differ between patients with benign and malignant prostatic disease. Thus, when investigating the role of prolactin in neoplastic prostatic growth in the human, it seems necessary to investigate receptor-mediated prostatic tumor responsiveness, and interferences with androgen converting enzymes on a cellular level, rather than circulating prolactin concentrations.

Pulsatile secretion of prolactin in the male rat after pimozide administration is not due to pulsatile inhibition of PIF secretion

Sequential blood samples were taken every 2 min from intact male rats implanted with a permanent indwelling right atrial cannula. The relationship between pimozide dose and prolactin secreation was established by administering graded doses of pimozide (30–3000 μg/kg) as a single bolus injection through the indwelling cannula. The maximum response of prolactin secretion was achieved with 300 μg/kg pimozide. Higher doses of pimozide did not raise further the circulating prolactin concentration suggesting that the receptors for the presumed prolactin inhibiting factor (PIF) were blocked completely at this dose. Marked pulsatile fluctuations in circulating prolactin concentration were observed after administration of pimozide, at all dosages, or of another ‘specific’ dopaminergic receptor blocking agent, d-butaclamol. Since we assume that PIF receptors are completely blocked by the higher doses of pimozide, we conclude that this pulsatile secretion of prolactin cannot be due to the inhibition of PIF secretion but may be due either to the stimulation of prolactin releasing factor (PRF) secretion, or to an inherent rhythmicity in the prolactin secreting cells.

Effect of Benztropine on Haloperidol-Induced Prolactin Secretion

The effect of benztropine on haloperidol-induced prolactin secretion was investigated in 10 normal male volunteers. Benztropine had no effect on basal prolactin secretion but significantly enhanced the increased induced by haloperidol. The magnitude of the enhancement, however, was relatively small. These data suggest that in man cholinergic mechanisms have no effect on basal prolactin secretion but exert a weak inhibitory effect under conditions of dopamine receptor blockade. Differences in intrinsic anticholinergic properties may account for some of the variations in potency of different neuroleptics in increasing circulating prolactin concentrations.

Physiologic and pathologic profiles of circulating human prolactin

These radioimmunoassay studies were designed to test three hypotheses: (1) prolactin plays a major role in regulation of mammary function; (2) in the normal woman, prolactin is not a major obligatory factor in gonadal and menstrual cycle regulation; and (3) assessment of alterations in circulating prolactin concentration in response to stimulatory agents is useful in the evaluation of the hypothalamic-pituitary axis. (1) During pregnancy, serum prolactin increased progressively to term. Suckling resulted in a prompt increase in prolactin concentrations. (2) Daily prolactin determinations during the menstrual cycle revealed no cyclic pattern and no significant daily variation. (3) Increase in prolactin response to TRF in nine patients with idiopathic galactorrhea, eight of whom had amenorrhea, was similar to that observed in normal control subjects. Administration of l-dopa resulted in a decrease in prolactin in normal women, women with idiopathic galactorrhea, women following hypophysectomy, a patient with primary hypothyroidism, and in a patient with a chromophobe adenoma. These data support the validity of the first two hypotheses and suggest that further studies on the response to administration of hypothalamic-releasing factors may be useful clinical tools to distinguish neoplastic from nonneoplastic states.