FAILURE OF SODIUM LOADING OR DEFICIENCY TO AFFECT PLASMA PROLACTIN IN THE MALE RAT

ABSTRACT The relation between plasma prolactin (PRL) and sodium metabolism was studied in adult male rats. During the experiments attention was given to the avoidance of stress. Cannulated rats were infused with 2.5 ml 5 % NaCl over a 40 min period. Plasma PRL did not change during or up to 2 h after this infusion. Other rats were subjected to a sodium deficient diet for 3 weeks. This treatment which induced a marked rise in plasma aldosterone, did not cause a change in plasma PRL. It is concluded that PRL does not have an important role in the regulation of sodium balance.

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HYPOTHALAMIC-PITUITARY-TESTICULAR SYSTEM AND ADRENOCORTICAL FUNCTION

Acta Endocrinologica ◽

10.1530/acta.0.0810198 ◽

1976 ◽

Vol 81 (1) ◽

pp. 198-207 ◽

Cited By ~ 4

Author(s):

H. L. Verjans ◽

K. B. Eik-Nes

Keyword(s):

Adrenal Gland ◽

Blood Serum ◽

Adult Male ◽

Serum Levels ◽

Male Rats ◽

Intramuscular Administration ◽

Adrenocortical Function ◽

Male Rat ◽

Pituitary Secretion ◽

Slight Elevation

ABSTRACT Effect of intramuscular administration of ACTH or dexamethasone on blood serum levels of testosterone, LH and FSH was examined in intact and castrated, adult, male rats. Six IU ACTH or 1 mg dexamethasone were given daily for 7 days. Corticotrophin treatment had no influence on circulating testosterone, LH and FSH in intact or castrated male rats. Dexamethasone administration resulted in a slight elevation of serum FSH in intact animals but not in castrates. LH and testosterone remained normal in both intact and castrated animals injected with dexamethasone. Under our conditions of study the secretions from the adrenal gland appear to be insignificant for the regulation of pituitary secretion of gonadotrophins in the male rat.

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Somatostatin Inhibits prolactin secretion in the estradiol primed male rat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y81-165 ◽

1981 ◽

Vol 59 (10) ◽

pp. 1082-1088 ◽

Cited By ~ 15

Author(s):

G. R. Cooper ◽

S. H. Shin

Keyword(s):

Hormone Secretion ◽

Growth Hormone Secretion ◽

Blocking Agent ◽

Prolactin Secretion ◽

Male Rats ◽

Male Rat ◽

Dependent Manner ◽

Intact Male ◽

Plasma Prl

Somatostatin inhibits not only growth hormone secretion, but also the secretion of several other hormones. The role of somatostatin in prolactin (PRL) secretion has not been clearly demonstrated. The present study was undertaken to examine the effects of somatostatin on rat PRL secretion in several different circumstances where the circulating PRL level is elevated: (1) the estradiol primed intact male rat, (2) normal and (3) estradiol primed rats pretreated with pimozide, (4) normal and (5) estradiol primed hypophysectomized male rats with adenohypophyses grafted under the kidney capsule (HAG rat). Blood samples (70 μL) were taken every 2 min via an indwelling atrial cannula from conscious, unrestrained animals. In the estradiol primed intact rats, a bolus injection of somatostatin (10, 100, and 1000 μg/kg) lowered PRL levels in a dose-dependent manner. When the PRL concentration was elevated by the administration of pimozide (3 mg/kg), a dopaminergic receptor blocking agent, somatostatin was ineffective in decreasing plasma PRL concentration but the PRL concentration was lowered by somatostatin when the rat had been primed with estradiol. Somatostatin had no effect on the normal HAG rats, but lowered the plasma PRL concentration in the estradiol primed HAG rats. Since somatostatin inhibits PRL secretion only in the estradiol primed rats, it is suggested that estradiol priming creates a new environment, presumably via new or altered receptors, which can be inhibited by somatostatin.

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In vitro pituitary and testicular effects of the leptin-related synthetic peptide leptin(116-130) amide involve actions both similar to and distinct from those of the native leptin molecule in the adult rat

Acta Endocrinologica ◽

10.1530/eje.0.1420406 ◽

2000 ◽

pp. 406-410 ◽

Cited By ~ 32

Author(s):

M Tena-Sempere ◽

L Pinilla ◽

LC Gonzalez ◽

J Navarro ◽

C Dieguez ◽

...

Keyword(s):

Body Weight ◽

Adult Male ◽

Body Weight Gain ◽

Biologically Active ◽

Male Rats ◽

Male Rat ◽

Gh Secretion ◽

Adult Rat ◽

Testosterone Secretion

The obese gene (ob) product, leptin, has recently emerged as a key element in body weight homeostasis, neuroendocrine function and fertility. Identification of biologically active, readily synthesized fragments of the leptin molecule has drawn considerable attention, as they may provide a powerful tool for detailed characterization of the biological actions of leptin in different experimental settings. Recently, a fragment of mouse leptin protein comprising amino acids 116-130, termed leptin(116-130) amide, was shown to mimic the effects of the native molecule in terms of body weight gain and food intake, and to elicit LH and prolactin (PRL) secretion in vivo. As a continuation of our previous experimental work, the present study reports on the effects of leptin(116-130) amide on basal and stimulated testosterone secretion by adult rat testis in vitro. In addition, a comparison of the effects of human recombinant leptin and leptin(116-130) amide at the pituitary level on the patterns of LH, FSH, PRL and GH secretion is presented. As reported previously by our group, human recombinant leptin(10(-9)-10(-7)M) significantly inhibited both basal and human chorionic gonadotrophin (hCG)-stimulated testosterone secretion in vitro. Similarly, incubation of testicular tissue in the presence of increasing concentrations of leptin(116-130) amide (10(-9)-10(-5)M) resulted in a dose-dependent inhibition of basal and hCG-stimulated testosterone secretion; a reduction that was significant from a dose of 10(-7)M upwards. In addition, leptin(116-130) amide, at all doses tested (10(-9)-10(-5)M), significantly decreased LH and FSH secretion by incubated hemi-pituitaries from adult male rats. In contrast, in the same experimental protocol, recombinant leptin(10(-9)-10(-7)M) was ineffective in modulating LH and FSH release. Finally, neither recombinant leptin nor leptin(116-130) amide were able to change basal PRL and GH secretion in vitro. Our results confirm the ability of leptin, acting at the testicular level, to inhibit testosterone secretion, and map the effect to a domain of the leptin molecule that lies between amino acid residues 116 and 130. In addition, we provide evidence for a direct inhibitory action of leptin(116-130) amide on pituitary LH and FSH secretion, a phenomenon not observed for the native leptin molecule, in the adult male rat.

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

Journal of Endocrinology ◽

10.1677/joe.0.0680355 ◽

1976 ◽

Vol 68 (3) ◽

pp. 355-368 ◽

Cited By ~ 12

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.

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Male-specific suppression of hepatic microsomal UDP-glucuronosyl transferase activities toward sex hormones in the adult male rat administered bisphenol A

Biochemical Journal ◽

10.1042/bj20020804 ◽

2002 ◽

Vol 368 (3) ◽

pp. 783-788 ◽

Cited By ~ 22

Author(s):

Noriaki SHIBATA ◽

Junya MATSUMOTO ◽

Ken NAKADA ◽

Akira YUASA ◽

Hiroshi YOKOTA

Keyword(s):

Bisphenol A ◽

Mrna Expression ◽

Sex Hormones ◽

Adult Male ◽

Endocrine Disruptor ◽

Liver Microsomes ◽

Female Rats ◽

Male Rats ◽

Male Rat ◽

Blotting Analysis

Various adverse effects of endocrine disruptors on the reproductive organs of male animals have been reported. We found that UDP-glucuronosyltransferase (UGT) activities towards bisphenol A, testosterone and oestradiol were significantly decreased in liver microsomes prepared from adult male Wistar rats administered with the endocrine disruptor bisphenol A (1mg/2 days for 2 or 4 weeks). However, suppression of the transferase activities was not observed in female rats, even after bisphenol A treatment for 4 weeks. Diethylstilbestrol, which is well known as an endocrine disruptor, had the same effects, but p-cumylphenol had no effect on UGT activities towards sex hormones. Co-administration of an anti-oestrogen, tamoxifen, inhibited the suppression of the transferase activities by bisphenol A. Western blotting analysis showed that the amount of UGT2B1, an isoform of UGT which glucuronidates bisphenol A, was decreased in the rat liver microsomes by the treatment. Northern blotting analysis also indicated that UGT2B1 mRNA in the liver was decreased by bisphenol A treatment. The suppression of UGT activities, UGT2B1 protein and UGT2B1 mRNA expression did not occur in female rats. The results indicate that bisphenol A treatment reduces the mRNA expression of UGT2B1 and other UGT isoforms that mediate the glucuronidation of sex hormones in adult male rats, and this suggests that the endocrine balance may be disrupted by suppression of glucuronidation.

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Postreceptorial refractoriness of prolactin release mechanisms

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y83-105 ◽

1983 ◽

Vol 61 (7) ◽

pp. 676-684 ◽

Cited By ~ 4

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.

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Increased dopaminergic inhibition of prolactin in the hypoprolactinaemic IPL nude rat

Journal of Endocrinology ◽

10.1677/joe.0.1070325 ◽

1985 ◽

Vol 107 (3) ◽

pp. 325-329 ◽

Cited By ~ 4

Author(s):

H. Cohen ◽

I. Sabbagh ◽

P. Guillaumot ◽

J. Bertrand

Keyword(s):

Adult Male ◽

Physiological Saline ◽

Prolactin Secretion ◽

Male Rats ◽

Saline Control ◽

Plasma Prolactin ◽

Synthesis Inhibitor ◽

Nude Rat ◽

Prolactin Content ◽

Pituitary Prolactin

ABSTRACT In this study, aimed at investigating whether dopaminergic regulation of prolactin could be implicated in the hypoprolactinaemia observed in the IPL nude rat, dopaminergic inhibition of prolactin was suppressed using a catecholamine synthesis inhibitor α-methyltyrosine (MT) and a dopaminergic antagonist sulpiride. Adult male rats (IPL nude and normal) were injected through implanted atrial cannulae with either MT (250 mg/kg) or physiological saline (control). Rats were decapitated 2 h after the injection. Plasma prolactin levels, compared with basal values, increased by 15·6 ± 1·9 (s.e.m.)- and 5·89 ± 0·6-fold in IPL nude and normal rats respectively. This difference was highly significant. The pituitary prolactin content was decreased in both groups. In a second experiment, adult male IPL nude or normal rats were injected with either sulpiride (1 mg/kg) or saline and decapitated 2, 4, 8, 12, 14 and 24 h later. Plasma prolactin levels, compared with basal values, were increased in rats injected with sulpiride by 9·2 ± 1·8 and 3·4 ± 0·7-fold in IPL nude and normal rats respectively. The pituitary prolactin content was reduced more in IPL nude than in normal sulpiride-injected rats. These data suggest that prolactin secretion, as well as synthesis, is under an increased dopaminergic inhibition in the male IPL nude rat. J. Endocr. (1985) 107, 325–329

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Effect of ergocristine on prolactin secretion in the male rat with pituitaries grafted beneath the kidney capsule

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y79-195 ◽

1979 ◽

Vol 57 (11) ◽

pp. 1313-1316 ◽

Cited By ~ 4

Author(s):

S. H. Shin

Keyword(s):

Bolus Injection ◽

Decay Curve ◽

Prolactin Secretion ◽

Male Rats ◽

Male Rat ◽

Plasma Prolactin ◽

Elevated Plasma ◽

Kidney Capsule ◽

Fourfold Increase ◽

Single Bolus Injection

Male rats in which three pituitaries were grafted beneath the kidney capsule showed approximately a fourfold increase in circulating plasma prolactin concentration. The elevated plasma prolactin concentration did not remain at a constant level but fluctuated with time. The elevated prolactin concentration declined immediately after a single bolus injection of ergocristine (30 μg/kg). The slope of the prolactin decay curve, determined by sequential blood sampling, was parallel to a theoretical slope having a 7-min half-life. This result indicates that ergocristine blocked prolactin secretion immediately and completely as the decay curve (T1/2 = 6.5 min, confidence interval 4.5–11.3) resulting from the administration of ergocristine is the same as the endogenous prolactin decay curve (T1/2 = 7 min).

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