Serotonin stimulates prolactin secretion in the hypophysectomized adenohypophyseal grafted rat

1983 ◽  
Vol 102 (4) ◽  
pp. 511-516 ◽  
Author(s):  
K. M. Stobie ◽  
S. H. Shin
Keyword(s):  
Prolactin Secretion ◽  
Male Rats ◽  
Normal Male ◽  
Plasma Prolactin ◽  
Site Of Action ◽  
Plasma Prl ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract. Normal male, oestrogen (E2) primed male and hypophysectomized adenohypophyseal grafted male rats (HAG rats) were used in the experiments. Serotonin creatinine sulphate was injected as a bolus via an indwelling atrial cannula in the conscious free moving rat. Serotonin caused a dose-dependent increase in plasma prolactin (Prl) in normal (1, 3 and 10 mg/kg serotonin) and E2 primed (1 and 3 mg/kg serotonin) male rats that began immediately after injection and reached a peak within 12–15 min of injection. Oestrogen priming significantly increased the magnitude of the response to serotonin. To analyze the site of action of serotonin in the rat, serotonin (1 mg/kg) was injected into HAG rats. Serotonin increased plasma Prl in this rat preparation, indicating that serotonin acts directly on the ectopic pituitary.

Increased Urinary Excretion of Carnitine and Acylcarnitine by Mercuric Chloride Is Reversed by 2,3-Dimercapto-1-Propanesulfonic Acid in Rats

2010 ◽  
Vol 29 (3) ◽  
pp. 313-317
Author(s):  
Waleed A. Al-Madani ◽  
Nikhat J. Siddiqi ◽  
Abdullah S. Alhomida ◽  
Haseeb A. Khan ◽  
Ibrahim A. Arif ◽  
...  
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Mercuric Chloride ◽  
Free Carnitine ◽  
Male Rats ◽  
Significant Protection ◽  
Total Carnitine ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Wistar Male Rats

This investigation was aimed to study the effect of 2,3-dimercapto-1-propanesulfonic acid (DMPS) on mercuric chloride (HgCl2)-induced alterations in urinary excretion of various carnitine fractions including free carnitine (FC), acylcarnitine (AC), and total carnitine (TC). Different groups of Wistar male rats were treated with HgCl2 at the doses of 0.1, 0.5, 1.0, 2.0, and 3.0 mg/kg body weight, and the animals were sacrificed at 24 hours following HgCl2 injection. A separate batch of animals received HgCl2 (2 mg/kg) with or without DMPS (100 mg/kg) and sacrificed at 24 or 48 hours after dosing. Administration of HgCl2 resulted in statistically significant and dose-dependent increase in the urinary excretion of FC, AC, and TC in rats. However, the ratio of urinary AC:FC was significantly decreased by HgCl2. Pretreatment with DMPS offered statistically significant protection against HgCl2-induced alterations in various urinary carnitine fractions in rats.

Somatostatin Inhibits prolactin secretion in the estradiol primed male rat

1981 ◽  
Vol 59 (10) ◽  
pp. 1082-1088 ◽  
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.

Sensitizing effect of treatment with estrogens on TSH response to TRH in male rats.

1977 ◽  
Vol 233 (3) ◽  
pp. E235 ◽  
Author(s):  
A De Lean ◽  
F Labrie
Keyword(s):  
Estradiol Benzoate ◽  
Thyroid Stimulating Hormone ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Intact Male ◽  
Basal Plasma ◽  
Prolactin Content ◽  
High Doses ◽  
Sensitizing Effect ◽  
Plasma Prl

Daily administration of estradiol benzoate (10 microgram/100 g body wt) to intact male rats led to a twofold increase of the plasma TSH (thyroid-stimulating hormone) response to thyrotropin-releasing hormone (TRH) after 4 and 7 days of treatment whereas the basal plasma TSH level was not affected. The basal plasma PRL concentration and the PRL response to TRH were both markedly increased by estrogen treatment. The TSH pituitary content remained unchanged, whereas the PRL pituitary content increased in parallel with the effect on PRL secretion. Treatment with estrogens for 1 wk sensitized the TSH secretory response to low doses of TRH (10 ng), whereas no significant effect on the response was found at high doses of the neurohormone. The present data show that the stimulatory effect of estrogens on the TSH response to TRH is due to true sensitization of the thyrotrophs to the action of the neurohormone, whereas that on prolactin secretion can result partly from increased pituitary prolactin content.

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.

Prolactin secretion by mixed ACTH-prolactin pituitary adenoma cells in culture

1985 ◽  
Vol 108 (4) ◽  
pp. 456-463 ◽  
Author(s):  
Tohru Yamaji ◽  
Miyuki Ishibashi ◽  
Akira Teramoto ◽  
Takanori Fukushima
Keyword(s):  
Pituitary Adenoma ◽  
Cultured Cells ◽  
Prolactin Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Cells In Culture ◽  
Corticotrophin Releasing Factor ◽  
Lysine Vasopressin ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Corticotroph Adenomas

Abstract. To characterize the functional aspect of prolactin (Prl) cells coexisting with corticotroph adenomas, pituitary adenoma cells obtained from a patient with Cushing's disease and a patient with Nelson's syndrome, who were associated with hyperprolactinaemia, were cultured in monolayer and their Prl responses to various secretagogues were compared with those of prolactinoma cells in culture. Immunohistochemistry performed in one of these two adenomas demonstrated the presence of Prl-containing cells in addition to ACTH cells. When ACTH-Prl adenoma cells were exposed to ovine corticotrophin-releasing factor (CRF), a dose-dependent increase in both ACTH and Prl secretion was observed, which was blocked by coincubation with hydrocortisone. In contrast, no stimulatory effect of CRF on Prl release was observed in all of the experiments using prolactinoma cells. Thyrotrophin-releasing hormone, which consistently stimulated Prl secretion in ACTH-Prl adenomas, was effective in triggering Prl release in only 25% of the prolactinomas. Exposure of the cultured cells to lysine vasopressin, growth hormone-releasing factor and vasoactive intestinal peptide resulted in an increase in ACTH and Prl secretion in one ACTH-Prl adenoma, however, none of the prolactinomas responded to these stimuli to secrete Prl. Dopamine and somatostatin, on the other hand, uniformly suppressed Prl secretion from ACTH-Prl adenomas as well as from prolactinoma cells. These results suggest that the mode of Prl secretion by mixed ACTH-Prl pituitary adenomas is not identical to that by pure prolactinomas and is, at least in part, common to that of ACTH secretion.

Increased dopaminergic inhibition of prolactin in the hypoprolactinaemic IPL nude rat

1985 ◽  
Vol 107 (3) ◽  
pp. 325-329 ◽  
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

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

1979 ◽  
Vol 57 (11) ◽  
pp. 1313-1316 ◽  
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).

Role of the adrenal cortex in chronic stress-induced inhibition of prolactin secretion in male rats

1989 ◽  
Vol 120 (2) ◽  
pp. 269-273 ◽  
Author(s):  
A. López-Calderón ◽  
C. Ariznavarreta ◽  
M. D. Calderón ◽  
J. A. F. Tresguerres ◽  
M. I. Gonzalez-Quijano
Keyword(s):  
Adrenal Cortex ◽  
Chronic Stress ◽  
Immobilization Stress ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Prolonged Release ◽  
Plasma Prolactin

ABSTRACT The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids. Journal of Endocrinology (1989) 120, 269–273

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