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PubMed2006

Prolactin directly enhanced Na+/K+- and Ca2+-ATPase activities in the duodenum of female rats.

Prolactin has recently been shown to directly stimulate 2 components of the active duodenal calcium transport in female rats, i.e., solvent drag-induced and transcellular-active calcium transport. Since the basolateral Na(+)/K(+)- and Ca(2+)-ATPases, respectively, play important roles in these 2 transport mechanisms, the present study aimed to examine the direct actions of prolactin on the activities of both transporters in sexually mature female Wistar rats. The results showed that 200, 400, and 800 ng/mL prolactin produced a significant increase in the total ATPase activity of duodenal crude homogenate in a dose-dependent manner within 60 min (i.e., from a control value of 1.53 +/- 0.13 to 2.29 +/- 0.21 (p < 0.05), 2.68 +/- 0.19 (p < 0.01), and 3.92 +/- 0.33 (p < 0.001) micromol Pi x (mg protein)(-1) x min(-1), respectively). Activity of Na+/K+-ATPase was increased by 800 ng/mL prolactin from 0.17 +/- 0.03 to 1.18 +/- 0.29 micromol Pi x (mg protein)(-1) x min(-1) (p < 0.01). Prolactin at doses of 400 and 600 ng/mL also significantly increased the activities of Ca(2+)-ATPase in crude homogenate from a control value of 0.84 +/- 0.03 to 1.75 +/- 0.29 (p < 0.05), and 2.30 +/- 0.37 (p < 0.001) micromol Pi x (mg protein)(-1) x min(-1). When the crude homogenate was purified for the basolateral membrane, the Na(+)/K(+)-ATPase activities were elevated 10-fold. In the purified homogenate, 800 ng/mL prolactin increased Na(+)/K(+)-ATPase activity from 1.79 +/- 0.38 to 2.63 +/- 0.44 micromol Pi x (mg protein)(-1) x min(-1) (p < 0.05), and Ca(2+)-ATPase activity from 0.08 +/- 0.14 to 2.03 +/- 0.23 micromol Pi x (mg protein)(-1) x min-1 (p < 0.001). Because the apical calcium entry was the first important step for the transcellular active calcium transport, the brush border calcium uptake was also investigated in this study. We found that, 8 min after being directly exposed to 800 ng/mL prolactin, the brush border calcium uptake into the duodenal epithelial cells was increased from 0.31 +/- 0.02 to 0.80 +/- 0.28 nmol x (mg protein)(-1) (p < 0.05). It was concluded that prolactin directly and rapidly enhanced the brush border calcium uptake as well as the activities of the basolateral Na(+)/K(+)- and Ca(2+)-ATPases in the duodenal epithelium of female rats. These findings explained the mechanisms by which prolactin stimulated duodenal active calcium absorption.

Animals↗
PubMed1984

Brief decreases in dopamine result in surges of prolactin secretion in monkeys.

We have reported previously that the amount of dopamine in hypophysial stalk blood was sufficient to account for tonic hypothalamic inhibition of prolactin secretion in rhesus monkeys. In the present study we determined the effect on prolactin secretion of decreases in dopamine. When hypophysial stalk-transected, estrogen-treated monkeys were infused with dopamine at a rate (0.1 microgram X kg-1 X min-1) to achieve peripheral plasma concentrations similar to those previously measured in stalk blood, their elevated serum prolactin levels fell to base line (from 47.6 +/- 4.8 to 9.7 +/- 2.7 ng/ml, mean +/- SE, n = 4). Brief interruptions of the dopamine infusions lasting for 2.5, 5.0, or 7.5 min evoked rapid increases in serum prolactin concentrations (to 27.5 +/- 8.3, 52.9 +/- 3.6, and 58.9 +/- 8.1 ng/ml, respectively, at 10 min). Maximal prolactin levels were attained within 10 to 20 min after dopamine removal and serum prolactin remained elevated for an additional 35 to 150 min. Uninterrupted dopamine infusions of stalk-transected, estrogen-treated monkeys (n = 3) led to continuously suppressed prolactin values. These results demonstrate that brief decreases in dopamine lead to major increases in prolactin secretion. Thus, if a brief decrease in hypothalamic dopamine secretion occurs after a suckling stimulus in monkeys, as it does in rats, a decrease in dopamine secretion alone may account, in part, for suckling-induced prolactin secretion in monkeys.

Animals↗
PubMed1986

Activation of protein kinase C inhibits synthesis and release of decidual prolactin.

Activation of calcium-activated, phospholipid-dependent protein kinase C by diacylglycerol and phorbol esters has been shown to mediate release of hormones in many systems. To determine whether protein kinase C activation is also involved in the regulation of prolactin release from human decidua, we have examined the effects of various acylglycerols and phorbol esters on the synthesis and release of prolactin from cultured human decidual cells. sn-1,2-Dioctanoylglycerol (diC8), which is known to stimulate protein kinase C in other systems, inhibited prolactin release in a dose-dependent manner with maximal inhibition of 53.1% (P less than 0.01) at 100 microM. Diolein (100 microM), which also stimulates protein kinase C activity in some systems, inhibited prolactin release by 21.3% (P less than 0.05). Distearin and dipalmitin, which are much less effective in activating protein kinase C, and monopalmitin and tripalmitin, which do not activate protein kinase C, had no significant effect on prolactin release. Phorbol 12-myristate 13-acetate (PMA), phorbol 12,13-didecanoate, and 4 beta-phorbol 12,13-dibutyrate, which activate protein kinase C in other systems, also inhibited the release of prolactin, while the protein kinase C inactivate 4 alpha-phorbol-12,13-didecanoate was without effect. The inhibition of prolactin release was secondary to a decrease in prolactin synthesis. The amounts of prolactin synthesized by cells exposed to diC8 (300 microM) or PMA (10(-7) M) for 30 min were 56.3 and 50.0% less than that synthesized by control cells (P less than 0.01 in each instance).(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1994

Effects of LHRH and ANG II on prolactin stimulation are mediated by hypophysial AT1 receptor subtype.

We have used the nonpeptide angiotensin II (ANG II) receptor antagonists losartan (receptor subtype AT1) and PD-123319 (AT2) to determine the participation of ANG II receptor subtypes in luteinizing hormone-releasing hormone (LHRH)-induced prolactin release in a perifusion study using intact pituitaries in vitro. LHRH (1.85 x 10(-7) M) released prolactin consistently, whereas losartan (10(-5) M) abolished prolactin response without modifying basal prolactin or luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. PD-123319 (10(-5) M) had no effect on basal or LHRH-induced prolactin, LH, or FSH release. We also determined that the effect of ANG II on prolactin release was mediated by the same receptor subtype. In adenohypophysial cells dispersed in vitro ANG II (10(-8) M) released prolactin. Losartan (10(-7) and 10(-6) M), but not PD-123319, inhibited this effect. We conclude that in intact hypophyses of 15-day-old female rats the effect of LHRH on prolactin release is readily demonstrated. LHRH-induced prolactin release appears to be mediated by ANG II acting in a paracrine manner on AT1 receptors located on lactotrophs.

Angiotensin II↗
PubMed1981

Dopamine levels in hypophysial stalk plasma and prolactin levels in peripheral plasma of the lactating rat: effects of a simulated suckling stimulus.

Secretion of prolactin is tonically inhibited by hypothalamic release of dopamine into the hypophysial portal system. However, the role that changes in dopamine secretion play in altering prolactin secretion after physiologic stimuli is still unknown. The present study was designed to investigate changes in dopamine release into stalk blood during sucking-induced release of prolactin. An increase in prolactin secretion was induced in urethane-anesthetized, lactating rats by a 15-min electrical stimulation of an isolated mammary nerve trunk. This procedure induced a rapid increase in prolactin secretion, and a 7-fold increase in prolactin concentrations was observed within 20-30 min after stimulation began. In unstimulated control rats, prolactin levels remained at baseline values during the period of observation. Then, we measured the effect of this stimulus on the concentration of dopamine in hypophysial stalk plasma. Dopamine concentrations in hypophysial stalk plasma, collected at 15-min intervals before, during and after mammary nerve stimulation, decreased significantly by 20% during stimulation, returned to prestimulation values, and then increased significantly by 20% at 45-60 min. In control rats, no changes in dopamine concentrations were observed. These results demonstrate that a simple, inverse relationship between dopamine secretion and prolactin secretion does not exist during suckling. However, the observed decrease in dopamine secretion during mammary nerve stimulation may be an integral part of a complex mechanism, including other hypothalamic hormones, that lead to the release of prolactin.

Animals↗
PubMed1982

Suppression of prolactin secretion by benzodiazepines in vivo.

Administration of benzodiazepines to male or female rats was observed to inhibit prolactin release. Basal secretion of prolactin was only slightly suppressed with the highest dose of benzodiazepines; however, the rise in prolactin release following a stimulus was prevented even at low doses (0.1-1 mg/kg). The benzodiazepine diazepam blocked stress-induced prolactin release and, when given during the critical period of proestrus, the proestrus surge of prolactin. Diazepam administration also blunted the release of prolactin induced by dopaminergic receptor blockade following haloperidol, or by serotonergic receptor activation produced by fluoxetine, a serotonergic reuptake inhibitor plus 5-hydroxytryptophan, a serotonin precursor. Inhibition of prolactin release by benzodiazepine was dose related, and inhibition was still evident after repeated diazepam injection. The potency of three benzodiazepine analogues to inhibit prolactin release correlated with their potency to displace radiolabeled diazepam binding from brain membrane fractions or to induce other biological responses (clonazepam greater than diazepam greater than chlordiazepoxide). These actions of benzodiazepines on prolactin release are similar to those reported for gamma-aminobutyric acid (GABA). The hypothesis of a benzodiazepine GABA receptor complex suggests that GABA may be involved in these in vivo actions of diazepam.

5-Hydroxytryptophan↗
PubMed1984

Hypothalamic regulation of mating-induced prolactin release. Effect of electrical stimulation of the medial preoptic area in conscious female rats.

Lesions of the medial preoptic area (MPOA) induce nocturnal prolactin surges similar to those initiated by cervical stimulation (CS). These same lesions can abolish diurnal prolactin surges previously initiated by CS. Based on these results the MPOA has been suggested to contain two functionally dissimilar sets of neurons, one inhibitory for the nocturnal surge and the other stimulatory for the diurnal surge. The present study sought to demonstrate the existence of these neural elements by electrically stimulating the MPOA of conscious ovariectomized female rats during those times of day when these neurons would be most active. Serial blood samples were collected via cannula before, during and after the stimulation. Stimulation of the MPOA (01.00-05.00 h) on day 2 after CS inhibited the nocturnal surge of prolactin while sham MPOA stimulation of CS females did not disturb the nocturnal surge. MPOA stimulation in non-CS females had no effect upon prolactin secretion. Application of MPOA stimulation (15.00-19.00 h) to CS females also suppressed the diurnal surge of prolactin. Sham-stimulated CS females, however, secreted a diurnal surge peaking at 17.00 h. Basal prolactin levels were unaffected by MPOA stimulation (15.00-19.00 h) in non-CS females. The results from these experiments suggest that the MPOA contains neurons inhibitory for both the nocturnal and diurnal prolactin surges. In a further attempt to show a stimulatory role for the MPOA in prolactin regulation, MPOA stimulation was applied (15.00-19.00 h) to pentobarbital anesthetized non-CS females. Pentobarbital treatment allowed the MPOA stimulation to trigger two prolactin peaks, one at 16.00 h and the other at 19.00 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Prolactin-induced activation of tuberoinfundibular dopaminergic neurons: evidence for both a rapid 'tonic' and a delayed 'induction' component.

Results of previous studies have revealed that prolactin causes a delayed (12-16 h) increase in the rate of synthesis and turnover of dopamine (DA) in terminals of tuberoinfundibular (TI) neurons in the median eminence. Attempts to demonstrate a rapid in vivo action of prolactin on these neurons has been frustrated because pharmacological manipulations needed to make the biochemical measurements of TIDA neuronal activity (i.e., administration of alpha-methyltyrosine or NSD 1015) inhibit DA synthesis and thereby remove the tonic inhibitory control of DA on prolactin secretion. Thus, 'control' rates of synthesis and turnover of DA in terminals of TIDA neurons are actually values obtained in the presence of high circulating concentrations of prolactin. Results of the present in vivo studies demonstrate that there are two components to the activation of TIDA neurons by prolactin: a rapid 'tonic' component, which is responsive to acute changes in prolactin concentrations, and a delayed 'induction' component, which is activated by long-term changes in prolactin concentrations. Experimental observations which support this proposal are described below. Hypophysectomy or treatment with bromocriptine (a DA agonist) reduce circulating levels of prolactin and reduce the rate of DA synthesis in the median eminence. Intracerebroventricular (i.c.v.) administration of prolactin to these animals increases the rate of DA synthesis in the median eminence within 4 h (rapid 'tonic' component) and then causes a further increase after 12 h (delayed 'induction' component); only the latter component is blocked by treatment with cycloheximide, indicating the involvement in protein synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Responsiveness of tuberoinfundibular dopamine neurons in the aged female rat to the stimulatory actions of prolactin.

The autoregulatory feedback control of prolactin, which is mediated by tuberoinfundibular dopamine (DA) neurons, is altered in the aged rat; this is evidenced by increased circulating concentrations of prolactin and decreased activity of these neurons. In the present study the action of prolactin on tuberoinfundibular DA neurons in young and aged female rats was estimated by measuring the rate of DA synthesis (dopa accumulation following the administration of a decarboxylase inhibitor) in the median eminence. The rate of dopa accumulation in the median eminence of the aged (26 months) rat was reduced to 50-60% of that in the young (3 months) rat. The acute systemic administration of haloperidol, a DA antagonist which increases serum concentrations of prolactin or intracerebroventricular infusions of prolactin increased the rate of dopa accumulation in the median eminence of both young and aged rats by the same relative amount. The administration of haloperidol and prolactin increased the rate of DA synthesis to a greater extent in young than in aged rats. The administration of bromocriptine, a DA agonist which reduces serum concentrations of prolactin, decreased the rate of dopa accumulation in the median eminence of both young and aged rats. In young animals the intracerebroventricular administration of prolactin reversed the bromocriptine-induced decrease in DA synthesis in the median eminence after 4 h and caused a further increase after 12 h. Qualitatively similar effects were seen in the aged rats; however, prolactin-treated young rats had much higher levels of DA synthesis than aged rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

A possible role for lipoxygenase and epoxygenase arachidonate metabolites in prolactin release from pituitary cells.

We studied the effects of selected leukotrienes and hydroxyeicosatetraenoic acids (HETEs) on prolactin release from primary cultures of female rats anterior pituitary cells. Leukotrienes B4, C4, and D4 had no effect on basal prolactin release; however, they did enhance prolactin release that was stimulated by 1 or 5 nM thyrotropin-releasing hormone (TRH). Leukotriene C4 also enhanced prolactin release that was induced by phorbol myristate acetate (a protein kinase C activator) by maitotoxin (a calcium uptake stimulator), and by angiotensin II. 5-HETE, 12-HETE, and 15-HETE stimulated basal prolactin release at high concentrations (1 microM and greater), and 5-HETE and 12-HETE enhanced TRH- and angiotensin II-induced prolactin release at lower (nanomolar) concentrations as well. In order to determine the role of endogenous arachidonate metabolites in prolactin release, pituitary cell cultures were exposed to selected inhibitors of the 5-lipoxygenase enzyme, which metabolizes arachidonate to leukotrienes and 5-HETE, and to those of the epoxygenase enzyme, which metabolizes arachidonate to epoxyeicosatrienoic acids. These inhibitors decreased basal and secretagogue-induced prolactin release. In additional experiments, it was determined that TRH enhances the liberation from pituitary cells of arachidonate metabolites with high-performance liquid chromatography elution profiles similar to those of leukotriene C4 and omega-OH-leukotriene B4 (a metabolite of leukotriene B4) and the HETEs. Therefore, the production of leukotrienes, HETEs, and epoxyeicosatrienoic acids may be necessary for the normal release of prolactin.

Animals↗
PubMed1989

Effect of morphine and naloxone on plasma prolactin concentrations in the fetal sheep and pregnant ewe during late gestation.

This study investigated the effects of intrafetal morphine or naloxone administration on fetal and maternal plasma prolactin concentrations in the sheep during late pregnancy (117-143 days gestation). After intravenous morphine (3 mg/kg) there was a significant increase (p less than 0.05) in fetal plasma prolactin concentrations which was sustained for 180 min post-injection. There was no significant effect of either gestational age (125-133 days compared to 134-143 days gestation) or repeated administration (up to 3 treatments) of morphine on the fetal prolactin response to morphine. Intrafetal administration of naloxone (3.8 mg/kg bolus + 9.9 mg/kg/60 min), blocked the fetal prolactin response to morphine. Maternal plasma concentrations of prolactin were significantly increased (p less than 0.05) at 180 min after the intrafetal morphine bolus. When naloxone alone was infused, there was no change in fetal plasma prolactin concentrations, but there was a significant fall (p less than 0.05) in maternal plasma prolactin from 25 min after the start of the naloxone infusion. Thus, acute administration of morphine is associated with fetal and maternal hyperprolactinaemia. Although the endogenous opioids do not appear to mediate basal prolactin secretion in the fetus, they may have a role in the control of prolactin release in the pregnant ewe during late gestation.

Animals↗
PubMed1990

Modulatory effect of testosterone on the serotoninergic control of prolactin secretion in prepubertal rats.

The administration of 5-hydroxytryptophan (5-HTP) induced a prolactin release in male and female prepubertal rats at 20 days of age. This response was significantly higher in male than in female rats. Neonatal androgenization of the females significantly increased the release of prolactin induced by 5-HTP treatment compared to the values observed in males; thus, the neonatal exposure to androgens seems to be responsible for the sexual differences in the prolactin response to 5-HTP. In a second series of experiments the effect of this serotoninergic precursor on prolactin release in prepubertal (16, 26, and 30 days of age), peripubertal (45-day-old) and adult male rats was studied. Castration significantly decreased the prolactin release response to 5-HTP in prepubertal rats. The administration of testosterone to castrated rats markedly increased the prolactin release response to 5-HTP. Neither castration nor testosterone administration modified the prolactin response to 5-HTP in peripubertal and adult rats. These results appear to indicate that testosterone modulates the serotoninergic control of prolactin secretion during the prepubertal stage. The control of prolactin levels could be one of the mechanisms by which testosterone participates in the sexual maturation.

5-Hydroxytryptophan↗
PubMed1992

Mutually antagonistic effects of corticosterone and prolactin on rat lymphocyte proliferation.

The present study was designed to evaluate the immunological outcome resulting from experimental conditions involving different corticosterone and prolactin ratios in rats. One set of experiments was conducted to assess the effects of prolactin and corticosterone on the in vitro mitogen-induced proliferation of spleen lymphocytes from animals previously submitted to the manipulation of their glucocorticoid status throughout adrenalectomy (ADX) and/or exposure to acute stress. The results indicated that prolactin (5 x 10(-9) M) induced a significant increase in concanavalin A- (ConA) induced proliferation of splenocytes only from ADX-control, unstressed, rats. However, a lower dose of prolactin (10(-9) M) failed to influence lymphoproliferation. Corticosterone (2 x 10(-8) and 10(-7) M) induced a dose-dependent reduction in lymphocyte proliferation in all experimental groups. Further experiments were conducted to study the relative potency of prolactin to antagonize the in vitro corticosterone-induced suppression of ConA-stimulated lymphocytes. The results showed, on the one hand, that higher doses of prolactin (10(-8) and 5 x 10(-8) M) were effective in stimulating ConA-induced lymphocyte proliferation in control, undisturbed, rats. They also showed that when prolactin and corticosterone are simultaneously added to the cultures, the immunostimulatory effect induced by a dose of 10(-8) M of prolactin can either predominate over a weak suppressive action of corticosterone (2 x 10(-8) M) or totally antagonize to normal values a marked immunosuppression induced by a higher dose of corticosterone (10(-7) M). These data support the view that different ratios between prolactin and corticosterone concentrations can result in differential immunological outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1980

Acute effects of arginine vasotocin on plasma and pituitary levels of prolactin in the male rat: influence of urethane anesthesia.

The acute effects of arginine vasotocin (AVT), a putative pineal peptide, on plasma levels of prolactin were investigated in the unanesthetized, estrogen-progesterone-treated male rat. A 10-microgram s.c. injection resulted in significantly increased levels of prolactin while a 1-microgram injection depressed plasma levels of this hormone; an inhibition of release was further suggested by increased levels of pituitary prolactin in rats treated with the lower dose. The same dose administered subcutaneously to urethane-anesthetized rats had no significant effect on plasma prolactin titers while a 10-microgram dose was still stimulatory. In anesthetized rats, no dose of the AVT administered (1 ng to 10 micrograms, s.c., or 1 fg to 1 microgram, i.v.) resulted in inhibition of prolactin release. In the unanesthetized normal male rat, 5 micrograms AVT first increased and then decreased levels of prolactin. Urethane anesthesia appears to mask an inhibitory effect of AVT on plasma prolactin levels in these animal preparations. Since AVT is capable of decreasing plasma prolactin levels, this peptide might be involved in the depression of plasma prolactin levels which appears to (at least partially) mediate pineal-induced gonadal degeneration.

Anesthesia↗
PubMed1983

Respiratory distress syndrome in the newborn: relationship to serum prolactin, thyroxine, and sex.

Prolactin and thyroxine levels were measured by radioimmunoassay in cord blood of 61 premature infants of 26-36 weeks gestation. 30 of the infants subsequently developed respiratory distress syndrome (RDS). The infants who developed RDS had a mean cord prolactin level of 174.5 +/- 24.5 ng/ml and a mean cord thyroxine level of 5.9 +/- 0.4 micrograms/dl. In the 31 healthy infants, the mean cord prolactin and thyroxine levels were significantly higher (226.3 +/- 25.8 ng/ml and 7.1 +/- 0.4 micrograms/dl, respectively). The correlation coefficient between prolactin and thyroxine was r = 0.56 in infants with RDS (p less than 0.0008). Both prolactin and thyroxine correlated with gestational age in the RDS group (r = 0.71 and 0.47, respectively). Discriminant analysis shows that the correlation between prolactin and thyroxine is independent of gestational age (r2 = 0.32, p less than 0.05). There was no correlation between the levels of prolactin and thyroxine in infants without RDS. In the healthy group, the cord prolactin levels were significantly higher (p less than 0.01) in female (335.8 +/- 47.7 ng/ml) than in male infants (209 +/- 17.2 ng/ml). Premature infants who develop RDS have significantly lower thyroxine and prolactin levels in cord blood than infants who remain healthy.

Female↗
PubMed1984

Further evidence of prolactin production from human decidua and its transport across fetal membrane.

In this study the human decidua, chorion and amnion were incubated for short term. Only the decidua, secreted much prolactin clearly among them as a function of time. When the amounts of prolactin in the maternal blood, cord blood obtained from umbilical vein, or those released into decidual incubation medium were compared with the amniotic fluid prolactin levels, only the decidual prolactin correlated significantly with the amniotic fluid prolactin. The urine obtained from newborns showed a low concentration of prolactin. These results suggest that the origin of prolactin present in the amniotic fluid is not from the mother or fetus, but from the decidua which has the ability of producing prolactin, and that prolactin secreted from this tissue may be transported into the amniotic fluid through the fetal membrane and accumulated there.

Amnion↗
PubMed1981

Thyrotropin-releasing hormone stimulation of prolactin release from clonal rat pituitary cells: evidence for action independent of extracellular calcium.

Thyrotropin-releasing hormone (TRH) stimulates prolactin release and (45)Ca(2+) efflux from GH(3) cells, a clonal strain of rat pituitary cells. Elevation of extracellular K(+) also induces prolactin release and increases (45)Ca(2+) efflux from these cells. In this report, we distinguish between TRH and high K(+) as secretagogues and show that TRH-induced release of prolactin and (45)Ca(2+) is independent of the extracellular Ca(2+) concentration, but the effect of high K(+) on prolactin release and (45)Ca(2+) efflux is dependent on the concentration of Ca(2+) in the medium. The increment in (45)Ca(2+) efflux induced by 50 mM K(+) during perifusion was reduced in a concentration-dependent manner by lowering extracellular Ca(2+) from 1,500 to 0.02 muM (by adding EGTA), whereas 1 muM TRH enhanced (45)Ca(2+) efflux similarly over the entire range of extracellular Ca(2+) concentrations. Although 50 mM K(+) caused release of 150 ng prolactin from 40 x 10(6) GH(3) cells exposed to 1,500 muM Ca(2+) (control), reduction of extracellular Ca(2+) to 2.8 muM decreased prolactin release caused by high K(+) to <3% of controls and no prolactin release was detected after exposure to 50 mM K(+) in medium with 0.02 muM free Ca(2+). In contrast, TRH caused release of 64 ng of prolactin from 40 x 10(6) GH(3) cells exposed to medium with 1,500 muM Ca(2+), and release caused by TRH was still 50 and 35% of control in medium with 2.8 and 0.02 muM Ca(2+), respectively. Furthermore, TRH transiently increased by 10-fold the fractional efflux of (45)Ca(2+) from GH(3) cells in static incubations with 1,500 or 3.5 muM Ca(2+), hereby confirming that the enhanced (45)Ca(2+) efflux caused by TRH in both low and high Ca(2+) medium was not an artifact of the perifusion system.Data obtained with chlortetracycline (CTC), a probe of membrane-bound Ca(2+), were concordant with those obtained by measuring (45)Ca(2+) efflux. Cellular fluorescence of CTC varied with the extracellular Ca(2+) concentration and the duration of incubation. TRH decreased the fluorescence of cell-associated CTC in a manner strongly suggesting stimulus-induced mobilization of Ca(2+), and this effect was still demonstrable in GH(3) cells incubated in 50 mM K(+). These data suggest that TRH acts to mobilize sequestered cell-associated Ca(2+) reflected as a (45)Ca(2+) efflux which is independent of the extracellular Ca(2+) concentration. Mobilization of sequestered Ca(2+) into the cytoplasm may elevate free intracellular Ca(2+) and serve to couple stimulation by TRH to secretion of prolactin.

Animals↗
PubMed1992

Serum prolactin levels in homosexual and bisexual men with HIV infection.

OBJECTIVE: Prolactin is a neurohormone that may be secreted in response to stress and also has regulatory effects on the immune system. Some, but not all, studies suggest that prolactin levels are higher than normal in persons with HIV infection. The authors measured prolactin levels in HIV-positive and HIV-negative homosexual and bisexual men to assess possible differences in levels and then examined relationships between prolactin level and measures of medical status, anxiety, depression, stress, and neuropsychological test performance. METHOD: Blood for prolactin level determination was obtained from 121 HIV-seropositive and 79 HIV-seronegative homosexual and bisexual men enrolled in a longitudinal study. The men also underwent a daylong assessment that included medical, immunological, psychiatric, psychosocial, psychosexual, and neuropsychological evaluations. RESULTS: There was no statistically significant difference in serum prolactin level among the seronegative men, the seropositive men with no or minimal physical symptoms, and the seropositive men with significant physical symptoms of HIV infection. Furthermore, within the HIV-seropositive group, the correlations between serum prolactin level and measures of depression, anxiety, stress, and neuropsychological test performance were all nonsignificant. CONCLUSIONS: Serum prolactin level does not seem to respond to HIV infection or to be related to stress or psychiatric symptoms in HIV-infected men. As none of the subjects had AIDS, the possibility cannot be ruled out that prolactin level increases in very late stages of HIV infection.

Adult↗