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Results for “hyperprolactinemia”

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PubMed1981

Pathogenesis of hyperprolactinemia in uremic rats.

Experiments have been carried out in order to clarify to what extent the absence of PRL renal catabolism in experimental renal insufficiency is responsible for the high PRL circulating levels. Furthermore, the relative contribution of the glomerular filtration rate and peritubular degradation to PRL renal clearance have been assessed. Circulating PRL basal levels were measured by RIA in sham-operated and intact control rats and in three uremic rat models: urine autoinfusion, bilateral ureteral ligation, and bilateral nephrectomy. Plasma PRL basal levels (nanograms per ml; mean +/- SEM) were increased in sham-operated rats (30.3 +/- 5.1) with respect to control animals (18.5 +/- 2.7; P less than 0.05). Bilaterally nephrectomized animals (66.4 +/- 16.4) and those with bilateral ureteral ligation (69.3 +/- 15.9) developed similar hyperprolactinemia, in contrast to urine-autoinfused rats (20.2 +/- 2.1; P less than 0.005) whose hormone levels were similar to those of control animals. Creatinine levels were markedly elevated and comparable in the three uremic rat groups. The results suggest that: 1) hyperprolactinemia in rats in acute renal insufficiency is due primarily to reduced renal function; 2) PRL renal catabolism in the rat requires a certain rate of glomerular filtration; and 3) PRL peritubular degradation does not seem to be relevant in PRL catabolism by rat kidney.

Acute Kidney Injury↗

PubMed1985

Hyperprolactinemia decreases the luteinizing hormone-releasing hormone concentration in pituitary portal plasma: a possible role for beta-endorphin as a mediator.

Hyperprolactinemia can reduce the LH secretion in rats, but the mechanism of the effect of PRL is not clear. We have investigated the actions of PRL on the secretion of LHRH and LH and the interaction among PRL, beta-endorphin (beta-EP), and LHRH. The effects of PRL on LHRH and LH secretion were studied in ovariectomized female rats after transplanting four anterior pituitaries to the right kidney capsule of each ovariectomized rat for 2-3 weeks. The level of PRL in rats with pituitary transplants was approximately 5 times higher than that in control rats. The concentration of LHRH in pituitary portal plasma of hyperprolactinemic rats was approximately 4 times lower than that in control rats. Hyperprolactinemic animals also showed lower plasma LH levels than the controls. Since beta-EP inhibits the secretion of LHRH, we have tested whether the reduced secretion of LHRH in hyperprolactinemic ovariectomized rats is associated with an increase in beta-EP activity. This was studied by measuring the concentration of beta-EP in pituitary portal plasma and the response of LHRH and LH to the opiate antagonist naloxone. The level of beta-EP-like immunoreactivity in pituitary portal plasma was significantly higher in hyperprolactinemic rats than in control animals. Naloxone (10 mg/kg, sc) increased both LHRH and LH concentrations in hyperprolactinemic rats, but not in control rats. The present results demonstrate that hyperprolactinemia can reduce LHRH release and suggest a possible involvement of beta-EP in the PRL inhibitory action on LHRH.

Animals↗

PubMed1985

Hyperprolactinemia inhibits gonadotropin-releasing hormone (GnRH) stimulation of the number of pituitary GnRH receptors.

Gonadotropin secretion is diminished in the presence of hyperprolactinemia, and previous studies have shown that PRL can reduce GnRH secretion and impair LH responses to GnRH. To investigate the mechanisms of the inhibitory effects of PRL on the pituitary, we administered intraarterial pulse injections of GnRH (25 ng/pulse every 30 min) to castrate testosterone-implanted male rats placed in restraint cages. Serum PRL, GnRH receptor (GnRH-R), and LH responses to GnRH were measured at intervals over 72 h. In control animals which received saline pulses, serum PRL was transiently elevated to the range of 100-150 ng/ml during the first 24 h, GnRH-R remained stable (approximately 300 fmol/mg protein) and serum LH was low (less than 10 ng/ml) throughout the 72 h. GnRH pulses in castrate testosterone-implanted animals increased GnRH-R to values (approximately 600 fmol/mg) similar to those in castrate controls (no testosterone implant, saline pulses) through 48 h, but GnRH-R declined to baseline values by 72 h in both groups. Serum LH responses to GnRH pulses were only present at 24 h. Administration of bromocriptine throughout the 72 h to immobilized castrate rats or to castrate testosterone-replaced animals treated with GnRH pulses suppressed serum PRL, and GnRH-R concentrations remained elevated through 72 h. Serum LH responses to GnRH pulses were 5- to 20-fold higher in bromocriptine-treated rats, and responses were present throughout the 72 h of the experiment. Delaying the start of bromocriptine treatment until 36 h (after the spontaneous PRL peak) resulted in reduced GnRH-R and LH responses at 72 h. Similarly, administration of ovine PRL (during the first 48 h) to bromocriptine-treated rats produced low GnRH-R concentrations at 72 h. Thus, the transient elevation of PRL seen in immobilized rats can inhibit the GnRH-stimulated increase in GnRH-R and is associated with reduced LH responses to GnRH. These results indicate that PRL has a direct inhibitory effect on the gonadotrope and suggest that impaired GnRH-R responses to GnRH are one of the mechanisms involved in the diminished gonadotropin secretion seen in hyperprolactinemia.

Animals↗

PubMed1975

Pituitary hormonal reserve in patients presenting hyperprolactinemia, intrasellar masses, and amenorrhea without galactorrhea.

The pituitary release of gonadotropins, prolactin, and TSH after the simultaneous intravenous administration of 50 mug LH-RH was 400 mug TRH was evaluated in 7 amenorrheic women with sellar enlargement and hyperprolactinemia. It was found that only minimal amounts of LH and FSH were released by LH-RH. All patients had elevated serum prolactin levels but TRH administration elicited negligible release of prolactin. This was in contrast to the normal TSH response to TRH in most of these women. It is concluded that intrasellar masses may be associated with hyperprolactinemia which does not necessarily cause galactorrhea and that impaired gonadotropin reserve correlates with the presence of amenorrhea.

Adult↗

PubMed1977

The effect of osmotic stimuli on prolactin secretion and renal water excretion in normal man and in chronic hyperprolactinemia.

An osmoregulatory role for prolactin (PRL) in man has been postulated, and PRL secretion has been reported to be influenced by osmotic stimuli. Clinical observation, however, does not support this notion. The effects of water loading, hypertonic saline infusion and nicotine on serum PRL and on renal water metabolism were investigated in 6 normal subjects and in 8 patients with chronic hyperprolactinemia (four with and four without demonstrable pituitary tumors). None of the patients had thyroid, adrenal or vasopressin deficiency. Renal walter handling in these patients was indistinguishable from normal. Likewise, serum PRL was not affected by the stimuli employed in either the normal subjects or the patients. No correlation between degree or duration of hyperprolactinemia and renal water metabolism was found. It is concluded that PRL is not an important osmoregulatory hormone in man.

Adult↗

PubMed1980

Correlation of hyperprolactinemia with altered plasma insulin and glucagon: similarity to effects of late human pregnancy.

Plasma glucose and insulin concentrations were measured during oral glucose and iv tolbutamide tolerance tests in nine women with hyperprolactinemia and the amenorrheagalactorrhea syndrome (AGS). Glucose tolerance curves, basal insulin levels, and postchallenge plasma insulin responses were significantly higher in AGS women compared to those in an age- and weight-matched control group. Fasting plasma glucagon concentrations were unaltered in AGS, but suppression of the hormone after oral glucose was greater and more prolonged relative to the control response. Oral glucose tolerance tests were performed on nine normal women during late pregnancy who had physiological hyperprolactinemia comparable to that in the AGS group. Glucose tolerance curves, exaggerated plasma insulin responses, and glucagon suppression resembled those observed in the AGS women. These results suggest that elevated plasma PRL concentrations may contribute to the development of hyperinsulinemia and accentuated glucagon suppression in response to glucose that is characteristic of late human pregnancy.

Adult↗

PubMed1981

Hyperprolactinemia is associated with increased immunoreactive somatomedin C in hypopituitarism.

Serum concentrations of immunoreactive somatomedin C were determined in 78 patients with pituitary tumors or craniopharyngiomas. Patients with large tumors, GH deficiency, and normal PRL levels (group 1) had low somatomedin C concentrations (mean, 0.23 U/ml; n = 23). Group 2 included patients with large PRL-secreting pituitary tumors and GH deficiency. This group had serum somatomedin C concentrations in the normal adult range (mean, 1.01 U/ml; n = 20). Patients with hyperprolactinemia and normal pituitary GH secretion (group 3) also had somatomedin C concentrations which were normal (mean, 1.47 U/ml; n = 17). As a group, these values were slightly greater than those of the GH-deficient patients with hyperprolactinemia (P less than 0.05), but not significantly different from a fourth group of patients with tumors, normal pituitary function, and normal PRL levels (mean somatomedin C, 1.40 U/ml; n = 18). It is concluded that significantly increased concentrations of human PRL have the capacity to raise serum somatomedin C concentrations into the normal range in individuals with GH deficiency. In patients with normal pituitary function, however, this weak stimulator of somatomedin C has no detectable effect.

Adolescent↗

PubMed1981

Effects of thyrotropin-releasing hormone and metoclopramide in patients with phenothiazine-induced hyperprolactinemia.

TRH and metoclopramide tests were performed in 10 female patients with presumed phenothiazine-induced hyperprolactinemia to define the serum PRL response to these agents. Our results show that the serum PRL response to metoclopramide is blunted in most patients with phenothiazine-induced hyperprolactinemia, and the serum PRL response to TRH is exaggerated in most patients during and 3 weeks after stopping phenothiazines.

Adult↗

PubMed1981

Maintained fertility in a patient with hyperprolactinemia due to big, big prolactin.

The heterogeneity of serum PRL in a hyperprolactinemic but fertile woman (Patient A) was studied by gel chromatography. Ninety percent of her PRL eluted with the void volume as "big, big" PRL and only 6% coincided with monomeric "little" PRL. Sera from a woman who had hyperprolactinemia associated with infertility (Patient B) and a normal woman (Patient C) exhibited the usual heterogeneous distribution, where 5% and 19%, respectively, eluted as big, big PRL and 76% and 65%, respectively, eluted as little PRL. Serial dilutions of the serum from Patient A displayed nonparallelism to the lines obtained from similar dilutions of both PRL standard and serum from a normal woman, suggesting possible immunological differences among the three forms of the circulating hormone. This finding, together with reports that suggest big, big PRL has a low receptor affinity, may account for the apparent lack of any biological effect upon Patient A from her sustained hyperprolactinemia.

Adult↗

PubMed1983

Absence of a suppressive effect of 2-hydroxyestrone on hyperprolactinemia in patients with prolactinomas before and after estradiol administration.

The effect of the infusion of 2-hydroxyestrone (125 micrograms/h for 8 h) on plasma PRL levels was investigated before and 64 h after the administration of 1 mg estradiol benzoate in five patients with PRL-secreting pituitary adenomas. There was no effect on the circulating PRL levels measured hourly for 8 h during both episodes of 2-hydroxyestrone infusion, but plasma LH and FSH levels were suppressed. Infusion of 2-hydroxyestrone in two hyperprolactinemic patients with craniopharyngeomas also did not change the circulating PRL levels. We conclude that: 1) 2-Hydroxyestrone does not suppress PRL levels in patients with prolactinomas. This is not caused by the low estrogenic state of these patients, because 2-hydroxyestrone remained ineffective after the administration of estradiol. 2-Hydroxyestrone was also not able to suppress the estradiol-induced stimulation of PRL release. 2) 2-Hydroxyestrone does not diminish PRL levels in patients with suprasellar tumors and hyperprolactinemia. Therefore, infusion of 2-hydroxyestrone cannot be used in the differential diagnosis of hypothalamic and tumoral hyperprolactinemia.

Adult↗

PubMed1983

Bone density in amenorrheic women with and without hyperprolactinemia.

To determine whether decreased bone density in patients with PRL-secreting pituitary tumors is specifically related to hyperprolactinemia or is a consequence of disordered pituitary-gonadal function common to all amenorrheic states, we measured the bone mineral content of the radius by photon absorptiometry in normal subjects, in women with amenorrhea and normal serum PRL levels, and in women with PRL-secreting pituitary tumors. The women did not differ significantly in mean age, height, weight, or serum calcium, phosphorous, gonadotropin, testosterone, vitamin D, or PTH concentrations, and all had normal renal and thyroid function. The bone mineral content in women with amenorrhea and normal serum PRL levels (0.91 +/- 0.02 g/cm) was not significantly different from that in control subjects (0.88 +/- 0.01 g/cm). Patients with PRL-secreting tumors studied 2-5 yr after transsphenoidal surgery had significantly diminished bone mineral content whether they were cured (0.82 +/- 0.02 g/cm) or had persistent amenorrhea and hyperprolactinemia (0.81 +/- 0.02 g/cm). Serum estradiol concentrations did not differ significantly in the four groups, and there was no correlation between estradiol concentration and bone mineral content or between PRL concentration and bone mineral content in the amenorrheic women. The presence of decreased bone mineral content in hyperprolactinemic patients suggests that PRL may have a direct effect on bone and may be another indication for early treatment of PRL-secreting pituitary tumors.

Adult↗

PubMed1983

Transient hyperprolactinemia: a correctable cause of idiopathic female infertility.

Frequent measurements of prolactin throughout the menstrual cycle were obtained in 48 women with regular menses and longstanding idiopathic infertility. Forty-five of the 48 patients (94%) had a small but significant transitory preovulatory elevation in their serum prolactin levels (hPRL). These transitory elevations in hPRL to 27-70 ng/ml lasted only one to three days and coincided with the preovulatory estradiol peak. When this transient hyperprolactinemia was suppressed by treatment with an appropriate, titrated dose of bromergocriptine, 18 patients (40%) conceived within one to three months. Evidently, this transitory, relatively mild hyperprolactinemia was not sufficient to interfere with follicular maturation, ovulation, or corpus luteum function, but it may impair fertilization and/or implantation.

Adult↗

PubMed1983

Different rebound rise in plasma prolactin during the postdopamine infusion phase in puerperal women and patients with pathological hyperprolactinemia.

Dopamine infused at a rate of 4 micrograms/kg . min for 120 min induced at the end of the infusion period a clear-cut and similar suppression of circulating PRL levels in normal and puerperal women as well as in patients with hyperprolactinemia either due to a tumor or of unknown etiology. At the discontinuation of the infusion there was a marked PRL rebound above baseline levels in normal subjects and a rapid return to basal levels in subjects with pathological hyperprolactinemia. In contrast, there was no increase in plasma PRL in puerperal women, in whom PRL levels remained suppressed during the whole postinfusion period. The reason(s) for this pattern in puerperal women is presently unknown, although previous estrogen loading of the lactotropes during pregnancy may be involved.

Adolescent↗

PubMed1985

Hyperprolactinemia induced by an estrogen-progesterone synergy: quantitative and temporal effects of estrogen priming in monkeys.

We evaluated the quantitative and temporal characteristics of the estrogen component of an estrogen-progesterone synergy, which can induce hyperprolactinemia in macaques. In Exp I, six groups of monkeys were treated for 2 weeks with various doses of estradiol benzoate (EB), which resulted in peripheral estradiol concentrations of 250-1500 pg/ml, followed by 2 weeks of combined estrogen and progesterone treatment. In each of the groups, regardless of the dosages of estradiol benzoate alone, PRL concentrations remained within normal limits (approximately 18 ng/ml). In contrast, during the subsequent period of combined EB and progesterone therapy, hyperprolactinemia developed. The resultant PRL concentrations were not dependent on the dose of EB administered. In Exp II, three groups of monkeys were treated with EB (25 micrograms/kg) alone for various intervals and subsequently with both EB and progesterone for 14 days. When initiation of progesterone therapy was preceded by a 9- or 6-day period of estrogen priming, PRL concentrations were significantly (P less than 0.05) elevated within 3-4 days; in contrast, when the EB and progesterone treatments were initiated simultaneously, 8 days elapsed before the PRL elevations were significant. In a third experiment, to determine whether decidualized endometrium accounted for the increased PRL levels following estrogen and progesterone treatment, a hysterectomized monkey was treated with EB followed by combined EB and progesterone treatment. The PRL response was not different from that of intact monkeys similarly treated. From these findings we conclude 1) that the estrogen-progesterone synergy promoting PRL secretion is not of endometrial origin; 2) that approximately 1 week of estrogen priming is required for progesterone to induce PRL secretion; 3) and that the mode of action of estrogen is not dose dependent, but, rather, is a threshold effect.

Animals↗

PubMed1991

Pulsatile prolactin secretion in hyperprolactinemia due to presumed pituitary stalk interruption.

PRL, like other anterior pituitary hormones, is normally secreted in a pulsatile fashion. However, it is not known whether such pulses depend on dopamine and/or other hypothalamic factors. This question can be addressed by investigating patients with large pituitary mass lesions, since such patients often have hyperprolactinemia due to disruption of normal hypothalamic input to the pituitary gland. Six such patients (5 with non-PRL-secreting tumors and 1 with a craniopharyngioma) and 11 healthy control subjects had PRL levels measured every 15 min over 24 h. PRL pulses were located by cluster analysis. All patients had PRL pulses of normal frequency, but increased amplitude. Circadian variation in PRL pulse amplitude, present in healthy women, was abolished in tumor patients. These results imply that normal pituitary levels of dopamine do not control the generation of PRL pulses. Instead, PRL pulses may arise from the pituitary gland, with pulse amplitude and circadian rhythm modulation by dopamine and other hypothalamic factors. Alternatively, the mild hyperprolactinemia associated with large hypothalamic-pituitary tumors may represent partial impairment of dopamine secretion, with sufficient pituitary dopamine levels to maintain normal PRL pulse frequency.

Circadian Rhythm↗

PubMed1985

[The mechanism of induction of ovulation by bromocriptine in euprolactinemic anovulation--the role of occult hyperprolactinemia in anovulation].

It has been well documented that ovulation was induced by Bromocriptine treatment in euprolactinemic anovulation. The present study has been carried out to clarify the underlying mechanism. 28 patients with euprolactinemia (PRL less than 25 ng/ml) were treated with a 5 mg daily administration of Bromocriptine. Ovulation was induced in 13 cases, which were determined by their BBT charts. In the ovulated cases, PRL secreting capacities were increased, determined by TRH administration. On the other hand, PRL secreting capacities were normal in the anovulated cases. The studies of the circadian secretion of PRL revealed that a nocturnal hyperprolactinemic state occurred for several hours in the ovulated cases, which was not seen in the anovulated cases. From these results, the mechanism of induction of ovulation by Bromocriptine in euprolactinemic anovulation exists on the suppression of the increased PRL secreting capacity, which may be related to the occulted hyperprolactinemia at night. Ovulated cases by Bromocriptine are seemingly euprolactinemia, but in truth they may be a kind of hyperprolactinemia.

Adult↗

PubMed1981

Elevated serum DHEA-S levels in association with hyperprolactinemia.

Serum DHEA-S levels were significantly higher in women with hyperprolactinemia than in normal women during the early follicular phase. When comparison was made of serum DHEA-S levels in hyper-and normoprolactinemic patients with secondary amenorrhea due to hypothalamic-pituitary failure, serum DHEA-S levels were significantly higher in hyperprolactinemic patients than in normoprolactinemic patients. This indicates elevated serum DHEA-S levels in association with hyperprolactinemia, but not with amenorrhea pe se.

Amenorrhea↗

PubMed1979

Lack of adrenal androgen stimulation by ACTH in extreme hyperprolactinemia.

Acute and prolonged alpha 1-24 corticotropin stimulation was performed on a treated chromophobe adenoma patient with partial ACTH deficiency and extreme hyperprolactinemia. Cortisol and aldosterone stimulated normally. However, the basal concentrations of androstenedione (A) and dehydroepiandrosterone (DHA) were low, and that of DHA-sulfate (DHAS) was undetectable. Furthermore, A and DHA did not stimulate normally, and DHAS did not stimulate at all. It has been claimed that adrenal androgen production is increased in hyperprolactinemia. However, the inability of prolactin (Prl) to maintain adrenal androgen (AA) secretion, with and without added ACTH, is demonstrated in this patient.

Adenoma, Chromophobe↗