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PubMed1980

Twenty-four hour pattern of prolactin levels in female rats subjected to transection of the mesencephalic raphe or ablation of the suprachiasmatic nuclei.

The present study was undertaken to evaluate the 24-hour periodicity in serum prolactin levels subsequent to transecting the ascending serotonergic system or ablating the suprachiasmatic nuclei (SCN) of adult (185 g) female rats. The ascending serotonergic system was transected at the level of the rostral mesencephalon using a 1.5 mm wide knife and the SCN was ablated with a modified Halász-Pupp knife. The effect of raphe transection (RT) or SCN ablation on the circadian rhythm in nonstress serum prolactin levels was assessed 45 days after surgery by measuring with radioimmunoassay the serum prolactin concentration in serial blood samples obtained from the tail vein of lightly restrained rats. Serum prolactin concentration in control and RT animals showed circadian periodicity; peak levels occurred during the midafternoon, 4 h prior to the dark phase of the lighting regime (lights on at 4 a.m., off at 6 p.m.). The amplitude of the fluctuations of both groups varied markedly and were related to the estrous cycle. However, RT animals showed a reduced amplitude in the rhythm. In controls peak prolactin levels on days of proestrus and estrus were 15-20 times higher than on days of diestrus. In contrast, serum prolactin levels in SCN-ablated rats did not vary with a circadian periodicity but rather showed random, low amplitude fluctuations. Reproductive cyclicity was also abolished by SCN ablation, i.e., SCN-ablated rats presented persistent vaginal cornification. These data indicate that circadian periodicity in serum prolactin levels is not compromised by sectioning the ascending serotonergic fibers but is abolished after ablating the SCN.

Animals↗
PubMed1980

Evidence that serotonin is involved in prolactin release by electrical stimulation of the medial basal hypothalamus in the rhesus monkey.

The possibility that serotonin plays a role in prolactin secretion after electrical stimulation of the rhesus medial basal hypothalamus (MBH) was investigated. Prolactin responses to electrical stimulation and intravenous injection of 0.5 and 1.0 micrograms of thyrotropin-releasing hormone (TRH) were evaluated before and after administration of methysergide (MES), a serotonin receptor blocker (2 mg orally every 12 h for 48 h), and bromocriptine (CB-154), a dopamine agonist (2.5 mg orally every 12 h for 48 h). Both electrical stimulation and TRH caused prompt increases in serum prolactin. Prestimulation (basal) prolactin levels in both drug-treated groups were not significantly lower than basal levels in control groups. Pretreatment with MES significantly attenuated the electrically induced release of prolactin but had no effect on the TRH-induced release; CB-154 blocked prolactin release induced by both types of stimulation. The study reported here has provided evidence of a possible role for hypothalamic serotinin in releasing pituitary prolactin.

Animals↗
PubMed1981

In vivo and in vitro interference of phosphatidylserine liposomes on prolactin secretion in the rat.

The effect of sonicated suspensions of phosphatidylserine (PS), an acidic phospholipid, was investigated on prolactin secretion utilizing in vivo and in vitro approaches. Acute and chronic administration of PS reduced plasma prolactin levels during different phases of circadian rhythms. The phospholipid was able to inhibit the plasma prolactin surge, which occurs in cycling female rats on the afternoon of proestrus. The time course of PS on prolactin secretion was characterized by a short latency (15 min) and a long duration of action (6 h). In rats with hypothalamic deafferentation PS partially reduced the increase of circulating prolactin induced by pretreatment with alpha-methyltyrosine. An inhibition of prolactin release was observed if anterior pituitary glands were incubated in presence of PS. This effect was prevented by the addition of the dopamine antagonist sulpiride to the medium. In conclusion, PS decreases prolactin secretion both in vivo and in vitro. The inhibition of the hormone secretion appears to be due to the action of PS at the level of the pituitary; however, a concomitant stimulatory action on the turnover of the tuberoinfundibular neurons cannot be ruled out.

Animals↗
PubMed1982

Vasopressin has a direct effect on prolactin release in male rats.

Prolactin-releasing (PRF) activity was found in Pitressin (a commercial extract from posterior pituitary for vasopressin). Injection of Pitressin into conscious free-moving rats implanted with a permanent atrial indwelling cannula, produced a transient increase in prolactin concentration in the circulation. In order to find out whether the PRF activity was due to vasopressin or to an unidentified component in the Pitressin, we tested synthetic lysine vasopressin and demonstrated that vasopressin (1 U/kg) elevated plasma prolactin concentration about threefold. In contrast, oxytocin (1 U/kg) did not alter the prolactin concentration. In order to find out whether the effect of vasopressin is a direct or indirect action, we tested the vasopressin effect on hypophysectomized rats which had previously been implanted with 2 adenohypophyses under the kidney capsule. Again this dose (2 U/kg) of vasopressin elevated circulating plasma prolactin. These experiments indicate that vasopressin can elevate circulating prolactin concentration in nonestrogen-primed normal male rats and that vasopressin also stimulates prolactin secretion from transplanted glands dissociated from direct hypothalamic control.

Animals↗
PubMed1982

Effect of chloroquine on thyroliberin interaction with clonal rat prolactin cells. Cytochemical correlates.

The lysosomotropic agent, chloroquine, has been used to investigate the implication of lysosomal activity and membrane traffic in TRH binding, TRH internalization and TRH-induced stimulation of prolactin secretion in a rat prolactin cell line (GH3/B6). Chloroquine by itself does not affect cell number, cell protein and basal prolactin secretion. It does not alter TRH binding and internalization as well as both effects of TRH on the stimulation of prolactin secretion, i.e., prolactin release and prolactin production. In contrast, chloroquine partially inhibits the spontaneous dissociation of (3H)TRH from cells previously loaded with (3H)TRH and reduces prolactin release following TRH withdrawal. In addition the kinetic pattern of the TRH dissociation is modified in a manner which suggests that TRH is bound to different intracellular compartments. Chloroquine, nevertheless, does not alter the TRH-induced down regulation of (3H)TRH binding sites. Electron microscopic observations and acid phosphatases localization reveal that chloroquine elicits a disorganization of the Golgi zone and accumulation of membrane whorls within large vacuoles. This suggests that the effects of chloroquine on TRH interaction with GH3 cells may be mediated by an inhibition of membrane recycling.

Acid Phosphatase↗
PubMed1982

Pharmacological evidence that serotonergic stimulation of prolactin secretion is mediated via the dorsal raphe nucleus.

Administration of the serotonin-releasing drug DL-p-chloroamphetamine (PCA) to rats caused a dose-dependent increase in plasma prolactin levels. The effect was maximal 2 h after administration. The effect of PCA was prevented by prior administration of the serotonin synthesis inhibitor p-chlorophenylalanine-methyl ester (PCPA). PCPA pretreatment did not prevent the increase in plasma prolactin levels after administration of the serotonin agonist quipazine which is consistent with a postsynaptic receptor interaction of quipazine. To determine which serotonergic neurons are involved, the prolactin responses to PCA were determined in rats sustaining lesions of the dorsal or median raphe nuclei. The lesions were produced in desmethylimipramine-pretreated rats by local injections of 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks prior to the PCA challenge. In rats with dorsal raphe lesions, the effect of PCA on prolactin secretion was significantly attenuated. In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion. In addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin secretion.

Animals↗
PubMed1983

Dopamine creates a physical barrier to inhibit prolactin release in mammotrophs of estradiol-primed male rats.

After finding that ergocristine and somatostatin can cause extensive changes in mammotroph ultrastructure within 2 min of administration, we chose dopamine, the putative physiological prolactin-inhibiting factor, to correlate ultrastructural changes to inhibition of prolactin release. In order to choose a dose of dopamine for this study we tested the effects of 2 doses of dopamine (10 and 1,000 micrograms/kg) on inhibition of prolactin release. The higher dose of dopamine (1,000 micrograms/kg) completely inhibited prolactin release immediately (in less than 2 min) and maintained complete blockage for a period of 14 min. For the ultrastructural study we injected dopamine (1,000 micrograms/kg) in the right atrium of conscious free-moving rats through indwelling cannulae, and killed the rats by decapitation 2 min after dopamine administration. The following changes in mammotrophs were observed after the dopamine treatment: (1) increased numbers of secretory granules, (2) peripheral relocation of rough endoplasmic reticulum, and (3) increased numbers of 'intracellular bodies' (putative prolactin granule disposal system) associated with secretory granules. Because these rapid ultrastructural changes have been observed after treatment with three different compounds (dopamine, somatostatin and ergocristine), we do not believe that they are the unique effect of any one compound but the common denominator of the three compounds, i.e., inhibition of prolactin secretion being closely linked to the ultrastructural changes. We thus propose that the extensive ultrastructural changes that occurred in such a short period of time following dopamine administration are the mechanism of inhibition of prolactin release.

Animals↗
PubMed1986

Female reproductive function and sexually dimorphic prolactin secretion in rats with lesions in the medial preoptic-anterior hypothalamic continuum.

The role played by the medial preoptic area-anterior hypothalamus (MPOA-AH) in the regulation of reproductive function of the female rat was examined in the first part of the present study. Extensive bilateral lesions placed in different locations of the MPOA-AH continuum resulted in three different patterns of vaginal smears. Lesions located most rostrally and dorsally, sparing the suprachiasmatic nuclei (SCN), resulted in series of successive pseudopregnancies. Lesions located more caudally and ventrally, still sparing the SCN, eventuated in regular oestrus cycles with only occasional pseudopregnancies. MPOA-AH lesions encroaching upon the SCN were associated with persistent vaginal cornification. MPOA-AH-lesioned females exhibiting repeated pseudopregnancies were capable of mating, conceiving, and giving birth. Parturition in these females was uniformly delayed by 1 day and was associated with a variable incidence of stillbirth, cannibalism of newborn, or incomplete placentophagy. As a rule, MPOA-lesioned mothers did not retrieve pups but they did show crouching behaviour and some of them even secreted milk. Thus, while the MPOA subserves in the regulation of oestrous cyclicity and maternal behaviour, it appears to play no essential role in mating behaviour or in ovarian function during pregnancy and lactation. The pattern of prolactin secretion in MPOA-AH-lesioned male and female rats was evaluated in the second part of this study. Both intact and orchidectomized males were incapable of generating nocturnal prolactin surges following extensive bilateral ablation of the MPOA-AH. On the other hand, 6 out of 9 ovariectomized MPOA-AH-lesioned females exhibited spontaneous nightly surges of prolactin. The absence of the surges in the remaining 3 females was associated with invasion of the lesion into the SCN and/or structures rostral to the MPOA. During the light period, prolactin levels remained within the basal range in all lesioned females, irrespective of the presence or the absence of the nocturnal surge. These lesioned ovariectomized females, in contrast to nonlesioned females, were incapable of producing a diurnal (afternoon) surge of prolactin in response to administration of oestrogen, though their basal prolactin levels were much higher than the levels seen in oestrogen-treated, nonlesioned castrated males. These results support the view that the MPOA is inhibitory to the nocturnal prolactin surge while stimulatory to the diurnal surge. The results also suggest that the male rat is functionally devoid of both a 'diurnal-surge centre' residing in the MPOA, and a 'nocturnal-surge centre' located outside the MPOA.

Animals↗
PubMed1986

Evidence that opioid peptides and dopamine participate in the suckling-induced release of prolactin in the ewe.

A pharmacological approach was used to study the involvement of opioid peptides and dopamine in mediating the suckling-induced release of prolactin in the lactating ewe (10-20 days post partum). To promote reliable and predictable suckling activity lambs were fitted with elasticated masks to prevent sucking for 4.5 h. After a 1-hour control period of frequent blood sampling, ewes were treated (i.v. injections every 5 min) for a further 75 min with either saline vehicle, an opioid antagonist (naloxone; 4.17 mg/5 min), a dopamine antagonist (metoclopramide; 1.25 mg/5 min), a mixture of naloxone + metoclopramide or a dopamine agonist (apomorphine; 6.6 mg/5 min). Blood was withdrawn at 5-min intervals for determination of plasma prolactin and luteinizing hormone (LH) by radioimmunoassay. Plasma LH concentrations (less than or equal to 1 microgram/l) were not significantly affected by any of the drug treatments and there was no evidence for an acute fall in LH associated with suckling- or TRH-induced increases in prolactin secretion. Naloxone significantly (p less than 0.05) reduced the mean incremental change in prolactin concentration (delta PRL) in response to suckling (+7 +/- 18 micrograms/ml) compared with saline-infused controls (+79 +/- 26 micrograms/ml), an effect which was completely reversed by combined treatment with naloxone and metoclopramide (+146 +/- 56 micrograms/ml). Metoclopramide alone raised basal prolactin levels by 46% (p less than 0.01) but did not affect delta PRL in response to suckling (+115 +/- 52 micrograms/ml). Neither naloxone, metoclopramide nor a combination of the two drugs affected the subsequent prolactin to TRH (10 micrograms). Apomorphine, however, completely abolished both the suckling- and TRH-induced release of prolactin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Age-dependent changes in the mechanisms controlling prolactin secretion and phosphatidylinositol turnover in male rats: effect of phosphatidylserine.

The present study was undertaken in order to better characterize the functional state of anterior pituitary gland in young and old rats by using prolactin secretion and incorporation of radioactive phosphate into phosphatidylinositol (PI) as markers. The in vitro incorporation of radiolabeled phosphate into anterior pituitary PI was significantly (p less than 0.01) greater in young (3-5 months) than in aged (24-25 months) male Sprague-Dawley rats. No significant difference was found in the incorporation by pituitary tissue of 32P into phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Also, the extent of prolactin secretion from isolated pituitary was significantly greater in young than in aged rats, while the prolactin pituitary content was significantly higher in aged animals. In vitro dopamine (DA) decreased the incorporation of 32P into PI, both in young and old pituitary glands, and inhibited prolactin secretion into the incubation medium. Brain cortex-phosphatidylserine (BC-PS), a pharmacologically active purified phospholipid, capable of stimulating the dopaminergic system in the hypothalamus and of decreasing prolactin secretion both in humans and rats in vitro and in vivo, inhibited the incorporation of labeled phosphate into PI of pituitary glands from either young or old rats, but did not alter the prolactin secretion from the glands incubated in vitro. Baseline prolactin plasma levels did not differ significantly between young and old rats either when blood was collected from the trunk after decapitation or underwent sampling from chronically cannulated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

Comparison of the regulation of carboxypeptidase E and prolactin in GH4C1 cells, a rat pituitary cell line.

The treatment of GH4C1 cells, a prolactin-producing rat anterior pituitary cell line, with estradiol (1 nM), insulin (300 nM) and epidermal growth factor (10 nM) has been previously shown to substantially increase both the intracellular level of prolactin, as well as the number of secretory granules. In this study, we examined the effect of this treatment on levels of carboxypeptidase E (CPE), a prohormone-processing enzyme. GH4C1 cells contain CPE mRNA and enzymatic activity. The secretion of both prolactin and CPE activity from GH4C1 cells is stimulated 10-fold by 50 mM KCl and 2- to 3-fold by 100 nM thyrotropin-releasing hormone, suggesting that these two proteins are contained in secretory granules. Treatment of GH4C1 cells with estradiol, insulin, and epidermal growth factor causes an increase in the intracellular level of CPE to approximately 2-fold of control values. This change is much smaller than the change in the level of prolactin: intracellular prolactin is increased 140-fold by the treatment. Kinetic analysis of the CPE activity indicates that the treatment does not alter the Km of substrate hydrolysis, with the change in activity the result of an increase in apparent Vmax. Northern blot analysis indicates that the level of CPE mRNA is not influenced (less than 10%) by the treatment, whereas the level of prolactin mRNA is increased 9-fold. These results indicate that CPE is not coordinately regulated with prolactin in the GH4C1 cell line, although some regulation of CPE activity does occur.

Animals↗
PubMed1992

Evidence that prolactin mediates the stimulatory effects of estrogen on tuberoinfundibular dopamine neurons in female rats.

The effects of ovariectomy and estrogen on prolactin secretion and/or the activity of tuberoinfundibular dopamine (TIDA) neurons were examined by either concurrently measuring concentrations of prolactin in plasma and 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence of female rats or by determining the rate of DA synthesis (accumulation of 3,4-dihydroxyphenylalanine (DOPA) after the administration of a decarboxylase inhibitor) in the median eminence. For comparison, concentrations of alpha-melanocyte-stimulating hormone (alpha MSH) in plasma and DOPAC in the intermediate lobe of the pituitary (an index of the activity of tuberohypophysial DA neurons) were also determined. Ovariectomy produced a time-dependent decrease in the accumulation of DOPA and the concentrations of DOPAC in the median eminence and prolactin in plasma with maximal effects occurring by 7 days. Estrogen administration to ovariectomized rats increased plasma prolactin and median eminence DOPAC concentrations to levels comparable to those in diestrous controls. In contrast, neither ovariectomy nor estrogen replacement altered the concentrations of alpha MSH in plasma or DOPAC in the intermediate lobe. Administration of the DA agonist bromocriptine blocked the ability of estrogen to increase plasma prolactin and median eminence DOPAC concentrations. Also, administration of antiserum to rat prolactin blocked the stimulatory action of estrogen on median eminence DOPAC concentrations. Taken together, these results indicate that the stimulatory effect of estrogen on the activity of TIDA neurons is mediated by prolactin.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1992

Effect of elevated serum prolactin concentrations on cytokine production and natural killer cell activity.

In vitro and in vivo studies in rodents and human suggested an immunostimulatory effect of prolactin. The aim of the present study was to determine the impact of chronically elevated serum prolactin concentrations on the immune system in patients with prolactinomas. For this purpose parameters of the humoral and cellular immune system were studied in seven patients with prolactinomas on two occasions (1) when their serum prolactin concentration had been normalized through treatment with dopamine agonists and (2) when their serum prolactin concentration was high. Serum concentrations of immunoglobulines, interleukin 1, 3 and 6, TNF-alpha, interferon-gamma and the soluble interleukin 2 receptor, leukocyte subsets and the natural killer cell activity were found to be within the normal range on both occasions, i.e. at normal and at high serum prolactin concentrations. The assumption could be made that long-lasting elevation of serum prolactin concentration induces adaptive changes when the acute stimulatory effects of prolactin on several parameters of the immune system have subsided.

Adult↗
PubMed1993

Opiate receptor subtype involvement in the stimulation of prolactin release by beta-endorphin in female rats.

The prolactin secretory response to beta-endorphin and the involvement of opiate receptor subtypes in this response was determined in both diestrous and postpartum, lactating female rats. The involvement of the mu-, delta- and/or kappa-site was determined by administering specific antagonists for each of these sites prior to beta-endorphin. beta-Funaltrexamine (beta-FNA, 1 or 5 micrograms) was administered to block mu-sites, ICI 154,129 (5, 10 or 25 micrograms) blocked delta-sites and nor-binaltorphimine (norBNI, 8 micrograms) blocked kappa-sites. The ability of beta-FNA and ICI 154,129 to block prolactin secretion following morphine administration was also determined. A dose response study for beta-endorphin indicated that beta-endorphin, at doses as low as 25 ng, was a potent stimulus for prolactin release producing an increase in prolactin that mimicked the suckling-induced prolactin increase. In addition, all three antagonists were capable of antagonizing the stimulatory effect of beta-endorphin in both diestrous and postpartum female rats. These results indicate that beta-endorphin is a potent stimulus for prolactin secretion and that these three opiate receptor subtypes interact to produce its stimulatory effect on prolactin release.

Animals↗
PubMed1993

Investigation of the role of 5-HT3 receptors in the secretion of prolactin, ACTH and renin.

The potential roles of central and peripheral 5-HT3 receptors in the secretion of prolactin, adrenocorticotropic hormone (ACTH), corticosterone and renin was investigated. Male rats received the 5-HT3 antagonist ondansetron (0, 0.1 or 1 mg/kg i.p.), 30 min prior to injections of the serotonin (5-HT) releaser, p-chloroamphetamine (PCA; 0, 3 or 8 mg/kg i.p.). Blood samples were collected 60 min after PCA for radioimmunoassays of plasma prolactin, ACTH, corticosterone and renin concentrations. PCA significantly elevated secretion of each of these hormones. Pretreatment with the 5-HT3 antagonist, ondansetron, significantly attenuated the PCA-induced elevation of prolactin secretion, suggesting that 5-HT3 receptors contribute to the serotonergic stimulation of prolactin secretion. Ondansetron did not modify effects of PCA on ACTH, corticosterone or renin secretion. To determine whether the 5-HT3 receptor role in prolactin secretion is mediated in the brain, the endocrine effects of intracerebroventricular (i.c.v.) injections of 5-HT (30 micrograms/kg) or the 5-HT3 agonist, 2-methylserotonin (1, 20 or 200 micrograms/kg) were evaluated. Both 5-HT and 2-methylserotonin significantly elevated plasma prolactin levels 15 min postinjection. However, ondansetron (1 mg/kg i.p.) did not antagonize these actions. Both 5-HT and 2-methylserotonin also increased plasma ACTH and corticosterone concentrations. Finally, 5-HT suppressed, while 2-methylserotonin stimulated renin secretion. None of the hormonal effects of i.c.v. injected 5-HT or 2-methylserotonin were altered by ondansetron. Thus, the results suggest that peripheral, but not central 5-HT3 receptors are involved in the stimulation of prolactin secretion. Furthermore, 5-HT3 receptors do not mediate the serotonergic stimulation of ACTH, corticosterone, or renin secretion.

Adrenocorticotropic Hormone↗
PubMed1993

Altered luteinizing hormone and prolactin responses to excitatory amino acids during lactation.

We have used excitatory amino acids as tools to elucidate changes in hypothalamic function associated with lactation, focusing on the regulation of luteinizing hormone (LH) and prolactin secretion. In these studies, we have compared the responsiveness to NMA (N-methyl-D,L-aspartate), an agonist for the N-methyl-D-aspartate (NMDA) receptor, with that of kainate, an agonist for another type of glutamate receptor, the kainate receptor. To address the issue of the permeability of the blood-brain barrier to either NMA or kainate, systemic and central administration of the drugs were compared. Four injections of either drug were administered at 10-min intervals to cycling or lactating rats suckling 8 pups. All of these treatment significantly stimulated LH secretion in cycling rats. However, neither systemic injections of NMA (40 mg/kg) or kainate (2.5-3.5 mg/kg), nor third-ventricular administration of NMA (2 micrograms/2 microliters) or kainate (0.2-0.3 micrograms/2 microliters) stimulated LH secretion during lactation. In contrast, LH responses to NMA were observed in lactating animals suckling 2 pups. These data demonstrate that the intensity of the suckling stimulus determines the degree of gonadotropin-releasing hormone (GnRH) neuronal inhibition during lactation. Recovery of the LH response to NMA in animals suckling 8 pups was not observed after treatment with RU 486 to block the effects of progesterone. Thus, the elevated levels of progesterone during lactation do not appear to play a role in inhibiting GnRH neuronal responsiveness. Removal of the 8-pup suckling stimulus for 24 h also did not restore the LH response to NMA. However, treatment with RU 486 and removal of the suckling stimulus for 24 h did restore LH responses to NMA, suggesting that progesterone may play a role in prolonging the recovery of GnRH neuronal responsiveness. The prolactin responses to NMA and kainate changed with the reproductive state of the animal and the site of administration. Central injections of either drug stimulated prolactin release in both cycling and lactating animals. In contrast, whereas systemic administration of NMA stimulated prolactin secretion in cycling animals, kainate had no effect. In the lactating animals, systemic administration of either drug inhibited prolactin secretion. Thus, the difference in the prolactin responses to systemic administration of the drugs may not only be due to a difference in the distribution of kainate and NMDA receptors but also to the steady state level of activity of the prolactin-releasing and -inhibiting factors which is determined by the reproductive state of the animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed1994

Ontogeny of angiotensin-II-induced prolactin release in vivo and in vitro in female and male rats.

The prolactin-releasing effect of angiotensin II (AII) was studied in the developing female and male rat in vivo and in vitro. AII (50 and 100 micrograms/100 g b.w.) was injected intraperitoneally to female and male rats aged 4, 12, 20 and 28 days and males aged 38 days. AII (10(-6) M) was also tested in pituitaries incubated in vitro from animals of both sexes aged 12, 20 and 28 days. In addition, as two subtypes of AII receptors have been characterized on the basis of displacement with specific AII antagonists, we used the nonpeptide AII receptor antagonists losartan (AT1 subtype) and PD 123319 (AT2 subtype) to determine the AII receptor subtype functionally involved in AII-induced prolactin secretion in vivo in 25-day-old male rats. The efficiency of the prolactin-releasing effect of AII in vivo increased with age, and first responses were observed at 20 days of age in both sexes. No sexual differences were encountered. On the other hand, AII-induced prolactin release from pituitaries incubated in vitro was first demonstrated at 12 days in females and at 20 days in males. The effect increased with age in both sexes, and, at 28 days, pituitaries from females released more prolactin in response to AII than those from males. Losartan (3 mg/kg) completely abolished AII (50 micrograms/100 g b.w.)-induced prolactin release in vivo, while PD 123319 (3 mg/kg) did not. This suggests that pituitary AT1 receptors are functionally involved in the prolactin release induced by AII in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1994

Cyclosporine modifies the pulsatile secretory patterns of prolactin and luteinizing hormone in normal and pituitary-grafted female rats.

This study was designed to examine whether cyclosporine (CyA) acts on the endocrine system by modifying the pulsatile secretion pattern of prolactin and LH. Both pituitary-grafted and sham-operated rats were submitted to a subcutaneous vehicle or CyA (5 mg/kg) treatment daily for 10 days beginning on the day of surgery. Pituitary grafting and/or CyA administration changed the pulsatile pattern of prolactin observed in sham-operated animals. The mean values of serum prolactin were significantly increased by pituitary grafting and the treatment with CyA further increased them. The mean half-life of prolactin was significantly increased in pituitary-grafted rats and was not changed by CyA administration, although it was decreased in sham-operated rats. The frequency of prolactin pulses was significantly decreased in pituitary-grafted as compared to sham-operated controls and was not further modified by CyA administration. However, in sham-operated rats a significant decrease of this parameter was observed. Duration of the prolactin peaks was significantly increased by pituitary grafting, and was not modified by CyA administration in any of the groups studied. The absolute amplitude of the prolactin peaks was significantly increased in pituitary-grafted as compared to sham-operated animals, and the treatment with CyA further increased this parameter in both groups. Mean values of LH were significantly increased in pituitary-grafted as compared to control rats. CyA administration significantly increased LH levels in sham-operated rats and decreased them in pituitary-grafted animals. The mean half-life, the pulse frequency and the duration of LH peaks were not modified by either pituitary grafting or CyA administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗