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PubMed1980

Prolactin receptors in the rat kidney.

Specific binding of 125I-labelled ovine prolactin iodinated by a lactoperoxidase method was demonstrated in crude membrane preparations of kidneys and adrenals of male Sprague-Dawley rats and livers from female rats. Membrane preparations derived from the 100,000 g fractions of tissue homogenates contained most of the specific prolactin binding. Kinetic and affinity characteristics of prolactin binding to kidney membranes were examined in detail. Maximal specific binding occurred after incubation for 30 h at room temperature. Scatchard analysis indicated that prolactin binding to kidney membranes was of high affinity (dissociation constant = 1.4 x 10(-10) mol/l) and similar to that for liver membranes, although kidney membranes from male rats bound approximately sixfold less prolactin/mg membrane protein than did liver membranes from female rats. Specific prolactin binding was demonstrated in both renal medulla and cortex. Autoradiography showed maximal prolactin binding activity in the epithelial cells of the proximal tubule and faint activity in the tubular cells throughout the nephron. Specificity of uptake by proximal tubular cells was indicated by the gross reduction in prolactin activity when excess ovine prolactin was administered simultaneously. The demonstration of specific binding sites for prolactin localized primarily in the proximal tubules was consistent with renal action of prolactin, predominantly on sodium metabolism.

Adrenal Glands↗
PubMed1985

Effects of 5-hydroxytryptamine uptake blockers on the release of LH and prolactin in several different experimental steroid models in the rat.

The effect of the 5-hydroxytryptamine (5-HT) uptake blockers on the surges of LH and prolactin has been investigated in pro-oestrous rats and various experimental models used frequently to study the effects of steroids on LH and prolactin secretion in female rats. The steroid models were: rats ovariectomized on dioestrus, injected immediately with oestradiol benzoate (OB) and at 12.00 h on the next day (presumptive pro-oestrus) with progesterone (model 1); long-term ovariectomized rats injected with a single injection of OB and 72 h later with either progesterone (model 2) or OB (model 3); long-term ovariectomized rats injected daily with OB (model 4). The uptake blockers alaproclate (3-30 mg/kg) and zimelidine (20 mg/kg) were injected and blood samples withdrawn from previously implanted intra-atrial cannulae. Plasma LH and prolactin concentrations were determined by radioimmunoassay. The present study confirmed that a surge of LH occurs at about 17.00-18.00 h of the presumptive day of pro-oestrus in model 1, at about 5 h after (approximately 17.00 h) the injection of either progesterone or the second injection of OB in models 2 and 3, and diurnally in model 4, and the simultaneous occurrence of a prolactin surge in models 2 and 4. A surge of prolactin at the same time as the LH surge was shown to occur also in models 1 and 3. Alaproclate (30 mg/kg) administered at 15.00 h delayed significantly the peak of the prolactin surge in the pro-oestrous rat and models 1, 3 and 4, and in the latter the magnitude of the prolactin surge was also significantly reduced. By contrast, the peak of the prolactin surge in model 2 was significantly prolonged by alaproclate. Alaproclate had no significant effect on either the timing or the magnitude of the LH surge in the pro-oestrous rat, and models 3 and 4. The peak of the LH surge was delayed by alaproclate in model 1 and abolished in model 2, providing further evidence for the possible importance of interactions between 5-HT and progesterone in neuroendocrine control. Zimelidine had no significant effect on either the LH or prolactin surge in the pro-oestrous rat and in models 1 and 2. These results show that normal 5-HT uptake is necessary for the normal timing and/or magnitude of the spontaneous and steroid-induced prolactin surge but is not essential for the normal timing and magnitude of the spontaneous surge of LH and the LH surge in some but not all steroid models.(ABSTRACT TRUNCATED AT 400 WORDS)

Alanine↗
PubMed1986

Prolactin stimulates Na+-K+-ATPase activity located in the outer renal medulla of the rat.

The effect of rat prolactin on rat renal Na+-K+-ATPase activity was investigated by a cytochemical technique. Rat prolactin caused stimulation of Na+-K+-ATPase activity only in the outer medulla of the kidney, and not in renal cortical structures. Peak enzyme activity in cultured rat renal segments occurred after tissue had been exposed to rat prolactin for 2 min, and the time of maximal stimulation did not vary with the concentration of prolactin. There was a curvilinear response in Na+-K+-ATPase activity over the rat prolactin concentration range, 0.04-40 ng/l, but higher prolactin concentrations caused inhibition of enzyme activity. Na+-K+-ATPase response was totally blocked by specific rat prolactin antiserum. Human prolactin had no consistent effect on rat medullary Na+-K+-ATPase activity. Addition of specific tri-iodothyronine and arginine vasopressin antisera to rat prolactin was without effect, confirming that the stimulatory action of rat prolactin on Na+-K+-ATPase was not due to contamination with these hormones which are known to stimulate this enzyme.

Animals↗
PubMed1986

Development and amplification of mid-afternoon surges of prolactin secretion in ovariectomized immature rats.

The immature female rat shows a mid-afternoon surge of prolactin secretion which reaches a maximum on the day of first pro-oestrus. The present experiments were undertaken to elucidate the mechanisms which underly the development of this prolactin discharge. Detailed plasma prolactin profiles were obtained from short-term (48 h) ovariectomized rats at 23, 28 or 37 days of age. In the two older groups, but not the youngest, a mid-afternoon surge of prolactin secretion occurred in spite of the absence of the ovaries. To exclude the possibility that such an apparent ovarian-independent discharge of prolactin was due to an oestradiol effect which persisted for 2 days following ovariectomy, another study was conducted using long-term ovariectomized animals. Plasma profiles were obtained from neonatally ovariectomized rats at ages equivalent to juvenile (26-28 days), peripubertal (38-41 days) or adult (46-49 days) phases of development. A mid-afternoon surge of prolactin secretion was observed in the majority of animals (eight out of twelve) irrespective of the interval after ovariectomy; this finding further indicates that in the female rat there is a centrally originated mid-afternoon episode of prolactin secretion which is expressed during juvenile development even in the absence of the ovaries. The relatively small magnitude of these ovarian-independent prolactin discharges (c.f. the preovulatory prolactin surge) suggested that in the intact animal they are amplified by ovarian secretions. To test this hypothesis, oestradiol-containing silicone elastomer capsules were implanted s.c. into juvenile rats, immediately after ovariectomy, and plasma prolactin profiles examined 2 days later (28 days of age).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Stress-induced prolactin release in female, male and androgenized rats: influence of progesterone treatment.

Ether stress applied at 10.00 h induced a 100% increase in serum prolactin in intact and ovariectomized androgenized rats. Ovariectomy significantly diminished the basal serum prolactin values observed in intact androgenized rats. Two doses of progesterone (5 mg) given to intact and ovariectomized androgenized rats 14 and 2 h before exposure to ether stress increased prolactin values in the control groups but completely prevented the effect of stress. Exposure to ether stress induced a 100% increase in serum prolactin values in androgenized rats with increased serum progesterone levels 4 days after the induction of ovulation and the luteal phase with human chorionic gonadotropin (hCG). A group of androgenized rats with induced maternal behaviour and which had been suckled for 6 days was given 100 i.u. hCG and suckled for another 6 days after the hCG-induced luteal phase had been established. The serum prolactin and progesterone values of these rats were significantly higher than those treated with hCG only and ether stress did not increase prolactin release. A greatly increased serum concentration of prolactin was obtained in pro-oestrous and oestrous virgin rats after exposure to ether stress. Serum prolactin was also increased by stress in male rats. Progesterone administration to these female and male rats prevented stress-induced prolactin release. To ascertain the part played by dopamine and serotonin in the effect of stress on prolactin release, groups of androgenized and oestrous female rats were treated with bromocriptine or p-chlorophenylalanine methylester hydrochloride (pCPA).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Influence of bromocriptine and oestrogen on prolactin synthesis, secretion and tumour growth in vivo in rats.

The effects of diethylstilboestrol implants and bromocriptine administration on serum prolactin concentrations, prolactin messenger RNA (mRNA) and pituitary tumour weight were examined. Intact female Fischer 344 rats were implanted s.c. with 10 mg diethylstilboestrol (DES) under light anaesthesia. All animals except the control group carried the implant for 7 weeks at which time the rats were subdivided into five groups: A, control; B, DES for 7 weeks; C, DES for 7 weeks followed by withdrawal of DES for 1 week; D, DES for 7 weeks followed by withdrawal of DES and administration of bromocriptine for 1 week; E, DES for 8 weeks with concurrent administration of bromocriptine during the last week. Serum concentrations of prolactin were measured by radioimmunoassay, prolactin mRNA concentrations were measured by dot-blot hybridization and sodium dodecylsulphate-polyacrylamide gel electrophoresis of the in-vitro translated mRNA. Pituitary growth was estimated by changes in pituitary weight and assessed by light and electron microscopic examination. Treatment with DES dramatically increased serum prolactin concentrations and prolactin mRNA and induced pituitary tumour formation as shown by histological changes. Withdrawal of DES for 1 week did not lead to a decrease in pituitary tumour weight but was accompanied by a decrease in serum prolactin concentrations and prolactin mRNA from peak concentrations although they remained significantly increased above controls. Treatment with bromocriptine after DES implants were removed led to a significant reduction in pituitary tumour weight and a decrease in serum prolactin concentrations and prolactin mRNA. Histology of the pituitary tumour after the bromocriptine treatment showed pituitary cells similar to those from normal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

In-vitro evidence for the autoregulation of prolactin secretion at the level of the pituitary gland in the rat.

The autoregulation of rat prolactin secretion at the level of the pituitary gland was investigated, using a static incubation system. The rate of prolactin secretion from the female anterior pituitary gland in vitro was found to be constant when the medium was changed at 20-min intervals. However, when the medium was left unchanged and secretory products were allowed to accumulate, prolactin secretion began to decline within 60 min. This effect was not observed with the male tissue, where the level of accumulated prolactin did not reach that at which the inhibition occurred using female tissue. The nature of the putative secretory product causing the inhibition of prolactin secretion was investigated. Exogenous bovine prolactin (1-4 mg/l) caused an inhibition of endogenous rat prolactin secretion. Inclusion of monoamine oxidase in unchanged medium, to prevent dopamine accumulation in the medium (a possible consequence of co-storage and co-secretion with prolactin granules), did not prevent the inhibition observed in the control incubation. We therefore conclude that in-vitro autoregulation of prolactin secretion can occur at the level of the pituitary gland, probably due to the accumulated prolactin having a feedback action on the lactotroph. This might be of physiological significance if localized concentrations of the hormone within the gland are high.

Animals↗
PubMed1988

Release of prolactin is independent of the secretion of thyrotrophin-releasing hormone into hypophysial portal blood of sheep.

In order to determine whether pituitary prolactin release was directly related to the secretion of TRH into hypophysial portal blood, serial portal and jugular venous blood samples were collected from seven lactating and three non-lactating ewes. In another experiment, samples were collected from five ovariectomized ewes while being exposed to an audio-visual stress and then later administered with chlorpromazine. Secretion of TRH was pulsatile in all ewes and independent of prolactin secretion; TRH pulses coincided with significant increases in prolactin secretion in only 15% of cases and only 29% of prolactin pulses were associated with TRH pulses. Sixty-seven per cent of suckling bouts were associated with increases in prolactin secretion, but only 22% of these were associated with significant increases in TRH secretion. Chlorpromazine increased prolactin levels fourfold but did not affect portal concentrations of TRH. Audio-visual stress was not a reliable method of causing prolactin release in this model. Mean portal concentrations of TRH and jugular concentrations of prolactin were not significantly correlated. These results show that hypothalamic TRH and pituitary prolactin are secreted independently in the sheep, implying that increases in prolactin release caused by suckling or chlorpromazine are not the direct result of increased TRH secretion.

Animals↗
PubMed1992

Requirement of oestrogens for the sensitivity of prolactin cells to vasoactive intestinal peptide in rats and man.

Vasoactive intestinal peptide (VIP) is a prolactin-releasing hormone which is involved in the multifactorial modulation of prolactin secretion in mammals. Intravenous injection of VIP (1 microgram/kg) to fertile women increased plasma prolactin levels and heart rate and reduced diastolic pressure. The same treatment to menopausal women caused similar cardiovascular effects but did not modify plasma prolactin levels. In contrast, TRH (200 micrograms, i.v.) induced a significant increase in plasma prolactin levels in both fertile and menopausal women. The relevance of oestrogens in affecting VIP-stimulated prolactin secretion was evaluated in vitro by measuring prolactin release from pituitary cells of control and ovariectomized rats. The sensitivity of rat mammotrophs to VIP, but not to TRH, was completely suppressed 3 or 4 weeks after ovariectomy. Furthermore, implantation of rats with a silastic capsule containing oestradiol-17 beta during ovariectomy, preserved the cell responsiveness to VIP. The prolactin-releasing property of VIP was also restored when pituitary cells from ovariectomized rats were cultured for 3 days in the presence of 10 nmol oestradiol-17 beta/l before being used for prolactin release experiments. The present study shows that the ability of prolactin-secreting cells to respond to the stimulatory action of VIP requires high levels of circulating oestrogens, both in man and rats.

Adult↗
PubMed1993

Dopamine D1 receptor analogues act centrally to stimulate prolactin secretion in ewes.

It is well known that prolactin secretion is inhibited by dopamine activity via the pituitary dopamine D2 receptor. Dopamine D1 receptor analogues also affect prolactin levels although the mechanisms and physiological significance are poorly understood. The present study of the ewe was undertaken to characterize the effects of the D1 receptor agonist SKF 38393 and antagonist SCH 23390 on prolactin in this species and to determine whether the prolactin response to both drugs requires an intact hypothalamo-pituitary axis. Ovariectomized ewes were injected intravenously with vehicle, 0.2, 2 or 20 mg SKF 38393 (D1 agonist) or SCH 23390 (D1 antagonist). At the 20 mg dose, plasma prolactin concentrations were significantly (P < 0.01) increased by each drug and returned within an hour to control levels. When injected directly into the lateral ventricles of the brain (intracerebroventricular (i.c.v.) injection), a 100-fold lower dose of SKF 38393 (0.2 mg; P < 0.05) was sufficient to stimulate prolactin secretion. In contrast, i.c.v. injection of SCH 23390 (0.02 and 0.2 mg) had no effect on prolactin levels and at no dose was there evidence for suppression of prolactin levels. These results are in accord with earlier studies in the rat which suggested that the D1 agonist stimulated prolactin secretion via a direct effect on central dopamine D1 receptors whereas the D1 antagonist interacted with the pituitary dopamine D2 receptor to increase prolactin secretion. In a further experiment this hypothesis was tested in hypothalamo-pituitary disconnected ewes which were infused with dopamine (0.5 microgram/kg per min) for 3 h.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Migratory fat deposition in European quail: a role for prolactin?

The present study addresses the role of prolactin as a regulator of migratory fattening in European quail (Coturnix coturnix). Plasma prolactin levels in captive birds undergoing migratory fattening in an outdoor aviary and in the laboratory were measured by radioimmunoassay with an antibody raised against recombinant-derived chicken prolactin. No strong association between prolactin and migratory fattening was apparent, and prolactin levels were more closely related to daylength, with the highest concentrations being reached on long days. Plasma prolactin profiles were similar in intact and castrated male quail. Prolactin was secreted in a daily rhythm, with the highest concentrations occurring early in the photophase. However, when birds were food-restricted for 50 days during a migratory phase, there was no difference in fat deposition between birds food-deprived for the first half of the daily photophase compared with those deprived for the second half. Fattening was reduced in the food-restricted birds relative to ad libitum-fed controls, but there was no difference in plasma prolactin levels between the groups. Injections of ovine prolactin (4 mg/kg) significantly increased food intake and body mass of birds maintained on long days, but there were no differences in fattening between birds injected in the morning compared with those injected in the afternoon. Collectively, these results do not support a major role for prolactin in the regulation of migratory fat deposition in European quail.

Adaptation, Physiological↗
PubMed2000

Interaction between substance P and TRH in the control of prolactin release.

Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.

Analysis of Variance↗
PubMed2003

Effects of prolactin administered to a perfused area of the skin of Angora goats.

It is suspected that prolactin may affect mohair growth; therefore, effects of infusing prolactin on mohair growth were investigated using a skin perfusion technique. Seven Angora wethers (average body weight, 30 +/- 3 kg) were implanted bilaterally with silicon catheters into the superficial branches of the deep circumflex iliac artery and vein. For the first 14 d of the experiment, animals were infused (2.4 mL/h) with prolactin (one side) or control (other side) into the deep circumflex iliac arteries. The infusion rate of prolactin was 2.21 mg/d and was calculated to triple prolactin blood concentration in the perfused region. The area of skin supplied by the deep circumflex iliac artery was approximately 240 cm2. Two weeks after the cessation of infusions, 100-cm2 areas within the perfused regions were shorn to determine mohair growth. Greasy and clean mohair production was decreased (P < 0.05) by prolactin compared with control (3.79 vs 4.62 and 3.02 vs 3.67 g/[100 cm2 x 28 d], respectively). Oxygen satura tion in blood hemoglobin from the deep circumflex iliac veins was greater (P < 0.02) on the side infused with prolactin than on the control side (75.1 vs 68.2%). Higher concentrations of methionine, lysine, valine, isoleucine, and leucine were observed in blood of the deep circumflex iliac vein on the side infused with prolactin vs that infused with control (P < 0.05). In conclusion, direct skin infusion with prolactin decreased mohair fiber synthesis by the skin and may have concomitantly lessened oxygen consumption. Thus, effects of increasing prolactin concentration approximately two-fold in the skin on mohair fiber growth may not be limited to simple competition for nutrients between skin and other tissues such as the mammary gland.

Administration, Topical↗
PubMed1996

No difference between micro- and macroprolactinomas in the prolactin responsiveness to metoclopramide and dopamine administration.

Differences between micro- and macroprolactinomas, as regards the prolactin secretory pattern in response to pharmacological challenges, have been reported in in vivo and in vitro models, and interpreted as being due to different dopaminergic regulation of prolactin release. In 32 patients with prolactin-secreting tumors, 19 with microprolactinomas and 13 with macroprolactinomas, and ten healthy volunteers, we evaluated the prolactin secretion in response to pharmacological manipulations of central dopaminergic tone. To this end, three tests were performed, in random order: (1) 4-h saline infusion; (2) 10 mg metoclopramide as i.v. bolus; (3) 4-h dopamine infusion (0.01 microgram/kg/min) with a 10-mg metoclopramide bolus given after the second hour of infusion. Dopamine infusion, compared to saline, caused a significant prolactin decrease in all the three groups of subjects, without significant difference between micro- and macroprolactinoma patients. In prolactinoma patients, administration of metoclopramide induced a significant rise in plasma prolactin which, however, was significantly lower than the one displayed by controls. Again, no difference was observed between the two groups of hyperprolactinemic patients. Dopamine infusion induced a significant and comparable increase in the prolactin response to metoclopramide in micro- and macroprolactinoma patients, while it was ineffective in control subjects. In conclusion, no differences appear to exist between micro- and macroprolactinoma patients as regards the prolactin secretory pattern during pharmacological modifications of the dopaminergic tone. A central dopaminergic defect and an increased prolactin turnover with attendant reduction of the intracellular hormone pool may both be involved in the reduced prolactin release following provocative stimuli in patients with prolactinoma.

Adolescent↗
PubMed2002

Predictive value of serum prolactin levels measured immediately after transsphenoidal surgery.

OBJECT: Prolactin-secreting pituitary adenomas may be managed by surgery, medication, radiotherapy, or observation. The authors reviewed a consecutive series of patients who were followed for at least 5 years after surgery to assess the prognostic significance of preoperative factors (tumor size and prolactin level) and an immediate postoperative factor (prolactin level obtained the morning after surgery) on long-term hormonal outcome, thereby clarifying the indications for surgical removal of tumor, the definition of successful treatment outcomes, and the nature of "recurrent" tumors. METHODS: Between 1979 and 1991, 241 patients with prolactinomas underwent transsphenoidal resection. Nineteen patients were lost to follow-up review, whereas the remaining 222 patients underwent measurement of their prolactin levels on postoperative Day 1 (POD 1), at 6 and 12 weeks, and every 6 months thereafter for a minimum of 5 years. On POD 1, prolactin levels in 133 patients (Group 1) were lower than 10 ng/ml, in 43 patients (Group 2) between 10 and 20 ng/ml, and in 46 patients (Group 3) higher than 20 ng/ml. At 6 and 12 weeks, normal prolactin levels (< or = 20 ng/ml) were measured in 132 (99%) of the 133 patients in Group 1 but only in 32 (74%) of the 43 patients in Group 2. By 5 years postoperatively, normal levels of prolactin were still measured in 130 patients (98%) in Group 1 compared with only five patients (12%) in Group 2. No patient with a prolactin level lower than 3 ng/ml on POD 1 was found to have an elevated hormone level at 5 years. The likelihood of a long-term chemical cure was greater for patients with microadenomas (91% cure rate) than for those with macroadenomas (33%). Preoperative prolactin levels also correlated with hormonal outcome. CONCLUSIONS: Prolactin levels lower than 10 ng/ml on POD 1 predict a long-term chemical cure in patients with microadenomas (100% cure rate) and those with macroadenomas (93% cure rate). In contrast, a cure is not likely to be obtained in patients with normal levels ranging between 10 and 20 ng/ml on POD 1 if they harbor macroadenomas (0% cure rate). A recurrence reported several years after surgery probably represents the presence of persistent tumor that was not originally removed. If the initial operation was performed by an experienced surgeon, however, reoperation is not likely to yield a chemical cure.

Adolescent↗
PubMed1986

Changes in pituitary prolactin responsiveness to TRH during pregnancy.

Prolactin plasma concentration during pregnancy was determined in rats treated with thyrotropin-releasing hormone (TRH). Day 0 of pregnancy was defined as the day sperm were first found in the vagina. All blood samples were obtained in unanesthetized rats which had previously received a cannula in the right common carotid. On Day 8 of pregnancy, plasma prolactin concentrations reached a peak between 2400 and 0800 hr (lights on from 0600 to 1800 hr). Injection of TRH (1 microgram/kg body wt) via the carotid artery increased plasma prolactin levels within 5 min. The largest increase occurred when TRH was given during the prolactin surge, whereas much smaller effects were found when TRH was given at the beginning or after the end of the surge period. Thus, the sensitivity of the prolactin cell to TRH appears to be the greatest when the secretory activity of the cell is high. It was then determined whether there was any change in the sensitivity of the prolactin cell to TRH after the prolactin surges had disappeared at midpregnancy. Injection of TRH between 1100 and 1200 hr increased prolactin less on Day 12 than on Day 8 of pregnancy. Since placental lactogen (PL) levels in the plasma are high on Day 12 compared to Day 8, and are inhibitory to prolactin secretion, it was reasoned that PL may be the factor which caused the reduced sensitivity to TRH. However, hysterectomy on Day 11 failed to increase the pituitary responsiveness to TRH the next day. In summary, these data indicate that the pituitary responsiveness to factors that stimulate prolactin, such as TRH, varies with relation to the time of pregnancy or presence of the nocturnal surge. What cellular mechanism is responsible for these sensitivity changes is not known.

Animals↗
PubMedDate not supplied

Plasma and tissue prolactin detection in colon carcinoma.

Serum concentrations of prolactin, a trophic hormone produced by the pituitary gland, have been shown to be raised in certain group of patients with cancer. Prolactin was detected in 0-20% of the colon cancer by immunohistochemistry and in plasma in 6-53% of the patients. These conflicting results do not support the hypothesis of an ectopic prolactin production by colon carcinoma. The aim of this study was to confirm the reported incidence of hyper-prolactinemia in colorectal cancer and to find further evidence for an ectopic prolactin production by the tumor. Thirty consecutive patients with colon carcinoma were studied. Before surgery all the patients underwent blood sample collection to assay plasma prolactin levels. All patients underwent colectomy. All the neoplastic specimens were tested with antiprolactin antibody. In none of the patients were significantly high preoperative levels of plasma prolactin found. Prolactin immunostaining was not identified in any of the tumor specimens. We could not confirm previous reports of frequent hyperprolactinemia in patients with cancer. This is the first report in which the incidence of both hyperprolactinemia and prolactin positive immunostaining was 0%. Our study was unable to demonstrate the synthesis of prolactin by colorectal cancers. The tumor is unlikely to be the source of hormone production. Our results suggest that circulating prolactin levels cannot be used as prognostic marker in patients with colon cancer.

Aged↗
PubMedDate not supplied

[Effect of prolactin on the regulation of osmotic processes across the fetoplacental membranes in vitro].

INTRODUCTION: The aim of this investigation was to point to the influence of minerals and total osmolality on regulation and secretion of prolactin in decidual tissue of the placenta and the role of prolactin in regulation of osmotic processes across the fetoplacental membrane. MATERIAL AND METHODS: Explants for the tissue culture have been obtained from pregnant women with normal pregnancy and delivery, between the 277 and 282 days of gestation. The investigation consisted of 4 repeated experiments. The parietal decidua and the corresponding chorion were separated from the amnion, rinsed in salt solution and cut into explants 0.2 g of weight. After a 2-hour period of preincubation in the control medium, 12 explants were incubated in the media of altered mineral and osmotic properties, whereas the 13-th in the control medium. Concentrations of prolactin following the 3-hour incubation in the medium was estimated by immunoenzymologic procedures. RESULTS: During the 3-hour incubation, the control explants secreted on average 75.4 +/- 5.23 micrograms/l of prolactin in the experiment repeated 4 times. The changes of Na+, Cl-, K+, Mg++, P- and HCO3- concentrations and of the total osmolality have not significantly influenced the synthesis of prolactin. In the medium with no Ca++, the value of secreted prolactin was 26.7 +/- 3.34 micrograms/l (p < 0.001); increase of the Ca++ concentration has not influenced the synthesis of prolactin. In the medium with increased concentration of H+ (pH = 7.00), the prolactin concentration was 50.9 +/- 2.9 micrograms/l (p < 0.001). CONCLUSION: The minerals--Na+, Cl-, K+, Mg++, P-, HCO3- and the total osmolality do not significantly influence the synthesis of prolactin in decidual-chorionic tissue. Certain quantities of Ca++ and optimal concentration of H+ are necessary for the synthesis of prolactin (PRL).

Bicarbonates↗