Postreceptorial refractoriness of prolactin release mechanisms

1983 ◽  
Vol 61 (7) ◽  
pp. 676-684 ◽  
Author(s):  
R. Collu ◽  
J. R. Ducharme ◽  
D. Eljarmak ◽  
A. M. Marchisio ◽  
J. Bertrand ◽  
...  
Keyword(s):  
Binding Sites ◽  
Immobilization Stress ◽  
Significant Rise ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Initial Value ◽  
Prolactin Release ◽  
Pituitary Glands ◽  
Plasma Prl

Whilc a first injection of the antidopaminergic benzamide drug, sulpiride, induced a large rise in plasma prolactin (PRL) levels in chronically cannulated adult male rats, a second injection given 2 h later was totally inactive although the pituitary content of the hormone was still 76% of the initial value. When the second injection was given 8 h after the first it was slightly effective, but when administered 24 h later it was as effective as the first. The second of two consecutive injections of haloperidol given at 2-h intervals, or an injection of morphine given 2 h after sulpiride, were incapable of inducing a release of PRL. Two hours after an injection of sulpiride, a 30-min period of immobilization stress induced a significant rise in plasma PRL levels. A significant rise in plasma PRL levels was also observed when larger doses of sulpiride were given 2 h after a first injection of the drug. Apomorphine was at least as effective an inhibitor of PRL secretion when given 2 h after sulpiride than when injected after saline. In vitro studies of dopaminergic binding sites revealed the presence, in pituitary glands of sulpiride-treated rats, of receptors not modified by the drug. These data suggest that the only plausible explanation for the ineffectiveness of the second of two consecutive injections of sulpiride is the development of a state of refractoriness of the mechanisms that subserve the release of PRL induced by suppression of the inhibitory dopaminergic tonus.

PLASMA PROLACTIN IN UNDISTURBED CANNULATED MALE RATS; EFFECTS OF PERPHENAZINE, FREQUENT SAMPLING, STRESS AND CASTRATION PLUS OESTRONE TREATMENT

1977 ◽  
Vol 84 (1) ◽  
pp. 51-61 ◽  
Author(s):  
John A. M. Mattheij ◽  
Thea A. van Pijkeren
Keyword(s):  
Significant Rise ◽  
Male Rats ◽  
Similar Response ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Free Sample ◽  
Normal Males ◽  
Plasma Prl ◽  
Frequent Sampling ◽  
Chronic Cannulation

ABSTRACT Blood was collected from undisturbed male rats by means of chronically indwelling intrajugular cannulae and the plasma prolactin (PRL) concentration was determined by a radioimmunoassay. The effect of perphenazine, frequent bleeding, handling and brief ether stress in normal males and of stress in castrated oestrone treated males was determined. The plasma PRL concentration in undisturbed intact males was low. Castration plus oestrone treatment for 3 or 7 weeks had little or no effect on the PRL concentration. Neither frequent blood sampling nor removal of 3 ml blood over a period of 5 h affected plasma PRL concentration. Intravenous administration of perphenazine caused a striking and prolonged increase in plasma PRL in intact males. Brief handling or mild ether stress caused a significant rise in PRL within 2 min in intact males; 15–20 min later PRL had returned to the undisturbed level. Brief ether stress in oestrone treated castrates induced a comparable pattern of prolactin release, although of greater magnitude. In these animals a second stress one hour later induced a similar response. It is concluded that chronic cannulation neither affects the unstressed prolactin level nor interferes with the ability of the adenohypophysis to release PRL. The results also indicate that when rats are handled a truly stress free sample can only be obtained when the blood is drawn within one minute after the initial disturbance of the animal. The evidence presented indicates that oestrone treatment increases the responsiveness of male rats to stress-induced PRL release.

Effect of [Asu,]eel calcitonin on prolactin release in normal subjects and patients with prolactinoma

1985 ◽  
Vol 108 (3) ◽  
pp. 297-304 ◽  
Author(s):  
Hidesuke Kaji ◽  
Kazuo Chihara ◽  
Naoto Minamitani ◽  
Hitoshi Kodama ◽  
Tetsuya Kita ◽  
...  
Keyword(s):  
Body Weight ◽  
Bolus Injection ◽  
Normal Subjects ◽  
Regular Insulin ◽  
Prolactin Release ◽  
Saline Administration ◽  
The Central Nervous System ◽  
Plasma Prl ◽  
Male Subjects

Abstract. The effect of [Asu]eel calcitonin (ECT), an equipotent analogue of eel CT, on prolactin (Prl) secretion was examined in 12 healthy male subjects and in 6 patients with prolactinoma. In healthy subjects, ECT (0.5 μg/kg body weight · h) or saline was infused for 2 h and TRH was injected iv as a bolus of 500 μg at 1 h of ECT or saline administration. ECT did not affect basal Prl levels during 1 h of infusion. TRH caused a significant increase of plasma Prl with peak values of 75.2 ± 11.6 ng/ml in ECT-infused subjects, which did not differ from those infused with saline (68.5 ± 8.3 ng/ml). Next, an iv bolus injection of regular insulin (0.1 U/kg body weight) was followed by an infusion of ECT or saline alone. Plasma Prl peaks after hypoglycaemic stress were significantly lower in ECT-infused subjects than those in saline-injected controls (ECT, 16.5 ± 3.1 vs 33.5 ± 9.6 ng/ml, P < 0.05). In patients with prolactinoma, basal levels of plasma Prl ranging from 42.0–4130 ng/ml failed to change during iv infusion of ECT. Moreover, ECT (10−9–10−6m) did not affect Prl release from prolactinoma tissues perifused in vitro. These findings suggest that ECT may not act directly on the pituitary to modify Prl release. Rather, peripherally administered ECT appears to suppress Prl release via the central nervous system.

Ontogeny of Angiotensin-II-Induced Prolactin Release in vivo and in vitro in Female and Male Rats

1994 ◽  
Vol 59 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Graciela S. Díaz-Torga ◽  
Damasia Becú-Villalobos ◽  
Carlos Libertun
Keyword(s):  
Angiotensin Ii ◽  
Male Rats ◽  
Prolactin Release

Vasopressin responses and receptors in the mesenteric vasculature of estrogen-treated rats

1986 ◽  
Vol 251 (5) ◽  
pp. H885-H889 ◽  
Author(s):  
J. St-Louis ◽  
A. Parent ◽  
R. Lariviere ◽  
E. L. Schiffrin
Keyword(s):  
Binding Sites ◽  
Pressor Response ◽  
Female Rats ◽  
Maximum Response ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Binding Characteristics ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed

The effect of treatment with estrogens on the biological activity of arginine8 vasopressin (AVP) in the in vitro perfused mesenteric vascular bed and on the binding characteristics of [3H]AVP on membranes prepared from the same vascular bed was studied. Female rats treated with estradiol (400 micrograms/24 h sc), compared with ovariectomized rats, had an increase in the maximum response to AVP (from 128 +/- 3 to 153 +/- 3 mmHg) in the perfused preparation and an increase in the density of AVP binding sites (from 402 to 732 fmol/mg protein) in the membrane preparation. In male rats, the injection of estradiol increased the maximum response to AVP (from 109 +/- 4 to 137 +/- 3 mmHg) and the density of AVP binding sites (from 289 to 519 fmol/mg protein). The effective concentration producing 50% of maximum response of AVP in the perfused preparation was higher in male than in female rats, while the Kd in the binding experiments was similar in the four experimental groups. Our results show that estrogens upregulate the number of AVP binding sites, leading to an increase in the pressor response to AVP in the rat mesenteric vascular bed.

Homologous and heterologous regulation of somatostatin-binding sites on chicken adenohypophysial membranes

1990 ◽  
Vol 127 (3) ◽  
pp. 417-425 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan ◽  
D. Attardo
Keyword(s):  
Pituitary Gland ◽  
Binding Sites ◽  
Recombinant Dna ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Caudal Lobe ◽  
Direct Inhibitory Effect ◽  
Pituitary Glands

ABSTRACT Binding of 125I-labelled [Tyr1]-somatostatin (125I-[Tyr1]-SRIF) to pituitary caudal lobe membranes was suppressed in immature chickens 1 and 2 h after i.v. administration of unlabelled SRIF at concentrations of 1–100 μg/kg. In-vitro preincubation of chicken pituitary glands for 0·5–4·0 h with 0·1 μmol SRIF/l similarly reduced the binding of 125I-[Tyr1]-SRIF to caudal lobe membrane preparations. After a 4-h incubation in 0·1 mmol SRIF/l, the withdrawal of SRIF from the incubation media was accompanied 4 h later by a partial recovery in the binding of 125I-[Tyr1]-SRIF to pituitary membranes. Passive immunoneutralization of endogenous SRIF resulted in a prompt (within 1 h) and sustained (for at least 24 h) suppression of 125I-[Tyr1]-SRIF binding to pituitary membranes. The i.m. administration of cysteamine (300 mg/kg) to 12-week-old birds depleted hypothalamic SRIF stores and decreased the density of 125I-[Tyr1]-SRIF-binding sites in the caudal and cephalic lobes of the chicken pituitary gland. The reduction in SRIF content and in SRIF-binding sites occurred within 1 h of cysteamine administration and was maintained for at least 24 h. In 6-week-old birds, cysteamine (300 mg/kg) administration suppressed pituitary binding of 125I-[Tyr1]-SRIF for at least 5 days. Circulati concentrations of GH were markedly decreased 1 and 4 h after cysteamine injection, but not after 24 h. Pituitary binding sites for 125I-[Tyr1]-SRIF were not affected by pretreatment of pituitary glands for 2–12 h in vitro with thyroxine or oestradiol-17β (1 nmol/l–10 μmol/l) or with ovine GH or recombinant DNA-derived chicken GH (1–100 μg/ml in vitro and 100–1000 μg/kg in vivo). Ovine prolactin, at concentrations of 1–100 μg/ml was also without effect on 125I-[Tyr1]-SRIF binding to pituitary membranes following a 2- or 4-h incubation with pituitary glands. Pituitary binding sites for 125I-[Tyr1]-SRIF were, however, increased after a 24-h incubation with 1 μmol tri-iodothyronine (T3)/l in vitro and 4 and 24 h after the administration of T3 (100–1000 μg/kg) in vivo. Although T3 had no direct inhibitory effect on 125I-[Tyr1]-SRIF binding to pituitary membranes, binding was suppressed 1 and 2 h after the in-vivo administration of T3 at concentrations of 100–1000 μg/kg. These results therefore demonstrate homologous and heterologous regulation of SRIF-binding sites in the chicken pituitary gland. Journal of Endocrinology (1990) 127, 417–425

BIOSYNTHESIS OF GONADOTROPHINS BY RAT PITUITARIES IN VITRO

1975 ◽  
Vol 66 (3) ◽  
pp. 369-374 ◽  
Author(s):  
MRIDULA CHOWDHURY ◽  
EMIL STEINBERGER
Keyword(s):  
Comparative Study ◽  
Anterior Pituitary ◽  
Male Rats ◽  
Leucine Incorporation ◽  
Experimental Conditions ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Endogenous Proteases ◽  
Pituitary Homogenate

SUMMARY A method has been developed for studying biosynthesis of FSH in the rat pituitary in vitro. Anterior pituitary glands were incubated with [3H]leucine; a specific and sensitive immunoprecipitation technique was used to isolate FSH from the pituitary homogenate. Total FSH content of the samples was measured by a double-antibody radioimmunoassay technique. Using this technique, a comparative study of LH and FSH synthesis in the same pituitary of adult male rats incubated for various intervals (0·5–6 h) was done. Increased incorporation of [3H]leucine into both LH and FSH with time was noted. The rate and amount of [3H]leucine incorporation into FSH was found to be higher than that into LH, indicating that either the rate of FSH synthesis is higher than that of LH or FSH has more leucine residues than LH. Greater susceptibility of LH to degradation by endogenous proteases during dialysis may also reflect less incorporation of [3H]leucine into LH. This method provides a reliable tool for evaluating FSH synthesis under various experimental conditions.

PROLACTIN STIMULATION TEST WITH PERPHENAZINE: AN EVALUATION OF PLASMA PROLACTIN LEVELS AND PITUITARY SECRETORY ACTIVITY IN THE RAT

1976 ◽  
Vol 68 (3) ◽  
pp. 355-368 ◽  
Author(s):  
A. A. VAN DER GUGTEN ◽  
P. C. SAHULEKA ◽  
G. H. VAN GALEN ◽  
H. G. KWA
Keyword(s):  
Adult Male ◽  
Secretory Activity ◽  
Female Rats ◽  
Male Rats ◽  
Plasma Prolactin ◽  
Prolactin Release ◽  
Oestrogen Treatment ◽  
Endocrine Status ◽  
Pituitary Prolactin ◽  
Single Plasma

SUMMARY Many investigations of the regulation of prolactin synthesis and release are based on single plasma prolactin determinations. The purpose of the present experiment was to ascertain whether groups of rats (i.e. young or adult, male or female animals, being either intact, gonadectomized or gonadectomized and treated with oestrone), differing in age and/or endocrine status, will react to a single dose of perphenazine by an acute release of pituitary prolactin in proportion to their initial plasma prolactin levels. No consistent relation existed between the classification of the twelve groups of rats into three categories of basal plasma prolactin levels (i.e. < 20, 25–50, > 125 ng/ml) and their response to perphenazine. Even though all groups showed a highly significant increase of plasma prolactin levels the magnitude of the maximum prolactin response at 30 min varied greatly within the groups of one category and thus was not related to the initial prolactin levels. The effect of 14 days of oestrone treatment in increasing plasma prolactin levels in gonadectomized animals was greatest in young and adult male rats, less in young females and not significant in adult females. The results obtained after perphenazine treatment in the latter group made it clear that the effect of oestrogen treatment on prolactin release can be completely blocked by increasing synthesis and/or release of the prolactin-release inhibiting factor (PIF). Since perphenazine induces decrease of pituitary prolactin and a concomitant increase of plasma prolactin levels through lowered PIF-action, the positive effect of oestrogens on prolactin release (as observed in gonadectomized male and young female rats) apparently is caused by a different mode of action. The implications of these findings for the regulation of prolactin release, as affected by the endocrine status of the rat, is discussed. Moreover, comparison of prolactin lost from the pituitary and gained in the circulation of the experimental animals, with amounts of prolactin that were observed to disappear from plasma during the experiment, provided suggestive evidence that the capacity to synthesize and/or eliminate prolactin, after a sudden provoked release of the hormone, differed among the groups. The rates of synthesis by the pituitary, of release from the pituitary into the circulation as well as of elimination of the hormone from the circulation (equally involved in determining actual plasma levels) are thought, therefore, to be far more important for the elucidation of prolactin regulation than single plasma prolactin determinations.

INFLUENCE OF STEROID SEX HORMONES ON THE F. S. H.-RELEASE BY RAT HYPOPHYSES IN VITRO

1961 ◽  
Vol 36 (4) ◽  
pp. 485-497 ◽  
Author(s):  
G. P. van Rees
Keyword(s):  
Sex Hormones ◽  
Female Rats ◽  
Male Rats ◽  
Intact Female ◽  
Intact Male ◽  
Incubation Experiments ◽  
Rat Pituitary ◽  
Pituitary Glands ◽  
Steroid Sex Hormones

ABSTRACT The hypothesis that steroid sex hormones influence pituitary F. S. H. by independent actions on its production and capacity of the gland to release it has been investigated by means of incubation experiments. During incubation, rat pituitary glands released considerable amounts of F. S. H. into the medium. Inactivation of F. S. H. during incubation could not be demonstrated; once (in females) some production of F. S. H. was even observed. The amount of F. S. H. which is released into the medium is influenced by the quantity of F. S. H. stored in the hypophyses. Hypophyses from male rats pretreated with oestradiol released relatively more F. S. H. into the medium than hypophyses from control animals. On the other hand, pretreatment with testosterone caused the pituitary glands to release less F. S. H. into the medium. In agreement with these results, hypophyses from intact male rats released relatively less F. S. H. than hypophyses from intact female rats. These facts support the hypothesis that androgens depress pituitary F. S. H.-secretion by inhibiting the capacity to release it, while oestrogens, which can even promote this property of the pituitary gland, also act by directly inhibiting its production.

scholarly journals Effects of dehydration on endocrine regulation of the electrolyte and fluid balance and atrial natriuretic peptide-binding sites in perinatally malnourished adult male rats

2002 ◽  
pp. 835-848 ◽  
Author(s):  
N Sebaai ◽  
J Lesage ◽  
A Alaoui ◽  
JP Dupouy ◽  
S Deloof
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Water Deprivation ◽  
Receptor Gene ◽  
Plasma Osmolality ◽  
Significant Rise ◽  
Male Rats ◽  
Receptor Density ◽  
D Values ◽  
Receptor Gene Expression

OBJECTIVE: The first aim of this work was to investigate, under basal conditions in adult male rats, the long-term consequences of perinatal maternal food restriction on the plasma concentrations of vasopressin (VP), aldosterone and atrial natriuretic peptide (ANP) and on plasma renin activity (PRA). Furthermore, under these same conditions, the hypothalamic VP gene expression as well as the density (B(max)), affinity (K(d)) and gene expression of ANP receptors were determined in kidneys and adrenals. The second aim of this work was to examine the responsiveness to dehydration in perinatally malnourished rats. Thus, the latter parameters were studied in these rats after 72 h water deprivation. METHODS: This study was conducted on 4-Month-old male rats from mothers exposed to 50% food restriction (FR50) during the last week of gestation and lactation and on age-matched control animals (C). At this stage, both C and FR50 rats were killed by decapitation between 0900 h and 1000 h in order to determine parameters under basal conditions or after 72 h water deprivation. Plasma VP, ANP and aldosterone levels and PRA were determined by radioimmunoassay. Hypothalamic VP gene expression was determined in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) by in situ hybridization. The B(max) and K(d) values of ANP receptors were evaluated from Scatchard plots. ANP receptor gene expression was determined by Northern blot analysis. RESULTS: Under basal conditions, perinatal malnutrition reduced body weight, absolute weight of kidneys and adrenals, and haematocrit. Compared with control rats, FR50 rats had significantly greater plasma VP and aldosterone levels but PRA, plasma ANP levels, plasma osmolality and hypothalamic VP gene expression were not significantly different. Perinatal malnutrition did not significantly affect glomerular ANP receptor density, but in adrenals it decreased both B(max) and K(d) values of ANP-B receptors (biological receptors) and increased B(max) of ANP-C receptors (clearance receptors). ANP-B(A) (receptor subtype A of ANP-B receptors) receptor gene expression was not significantly affected, whereas ANP-C receptor gene expression was enhanced in both adrenals and kidneys in FR50 rats. After 72 h dehydration, control rats showed a significant rise in haematocrit, plasma osmolality, PRA, circulating levels of VP and aldosterone and VP gene expression in both PVN and SON but showed a decrease in plasma ANP levels. B(max) of ANP-B receptors was decreased whereas B(max) of ANP-C receptors was enhanced in both adrenals and kidneys. ANP-B(A) receptor gene expression was not significantly affected in either kidneys or adrenals in dehydrated control rats. Similarly, ANP-C receptor gene expression was unaffected in kidneys whereas it was significantly enhanced in adrenals. In FR50 rats, the effects of water deprivation were qualitatively similar to those reported in controls concerning plasma parameters except for plasma VP levels which tended to rise (not significant) but this increase was only very slight compared with controls. Moreover, unlike controls, VP gene expression in both PVN and SON was not enhanced after dehydration in FR50 rats. In kidneys, dehydrated FR50 rats, like controls, upregulated ANP-C receptors, but they were unable to downregulate ANP-B receptors. In adrenals, unlike controls, FR50 rats enhanced ANP-B receptor density whereas they decreased both ANP-C receptor density and expression after 72 h dehydration. Similar to controls, the expression of ANP-B(A) receptors in both kidneys and adrenals as well as the expression of ANP-C receptors in kidneys, were unaffected in dehydrated FR50 rats. CONCLUSION: Perinatal malnutrition had long-lasting effects on regulation of the fluid and electrolyte balance under basal conditions. The main effects were a significant rise in circulating levels of VP and aldosterone, and changes in density of adrenal ANP-binding sites and ANP-C receptor gene expression in both adrenals and kidneys. Perinatal malnutrition also affects the responsiveness to water deprivation with alterations in both hypothalamic VP gene expression and regulation of ANP-binding sites.

scholarly journals Peptide YY (PYY)3–36 modulates thyrotropin secretion in rats

2006 ◽  
Vol 191 (2) ◽  
pp. 459-463 ◽  
Author(s):  
K J Oliveira ◽  
G S M Paula ◽  
R H Costa-e-Sousa ◽  
L L Souza ◽  
D C Moraes ◽  
...  
Keyword(s):  
Peptide Yy ◽  
Significant Rise ◽  
Gonadotropin Secretion ◽  
Gut Hormone ◽  
Pituitary Glands ◽  
Thyroid Axis ◽  
Dose Dependent Decrease ◽  
Serum Tsh

Peptide YY (PYY)3-36 is a gut-derived hormone, with a proposed role in central mediation of postprandial satiety signals, as well as in long-term energy balance. In addition, recently, the ability of the hormone to regulate gonadotropin secretion, acting at pituitary and at hypothalamus has been reported. Here, we examined PYY3-36 effects on thyrotropin (TSH) secretion, both in vitro and in vivo. PYY3-36-incubated rat pituitary glands showed a dose-dependent decrease in TSH release, with 44 and 62% reduction at 10−8 and 10−6 M (P < 0.05 and P < 0.001 respectively), and no alteration in TSH response to thyrotropin-releasing hormone. In vivo, PYY3-36 i.p. single injection in the doses of 3 or 30 cg/kg body weight, administered to rats fed ad libitum, was not able to change serum TSH after 15 or 30 min. However, in fasted rats, PYY3-36 at both doses elicited a significant rise (approximately twofold increase, P < 0.05) in serum TSH observed 15 min after the hormone injection. PYY3-36 treatment did not modify significantly serum T4, T3, or leptin. Therefore, in the present paper, we have demonstrated that the gut hormone PYY3-36 acts directly on the pituitary gland to inhibit TSH release, and in the fasting situation, in vivo, when serum PYY3-36 is reduced, the activity of thyroid axis is reduced as well. In such a situation, systemically injected PYY3-36 was able to acutely activate the thyrotrope axis, suggesting a new role for PYY3-36 as a regulator of the hypothalamic–pituitary–thyroid axis.

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