MECHANISM(S) BY WHICH ADRENALECTOMY AND CORTICOSTERONE INFLUENCE PROLACTIN RELEASE IN THE RAT

1980 ◽  
Vol 87 (1) ◽  
pp. 131-NP ◽  
Author(s):  
F. C. LEUNG ◽  
H. T. CHEN ◽  
S. J. VERKAIK ◽  
R. W. STEGER ◽  
J. J. PELUSO ◽  
...  
Keyword(s):  
Serum Levels ◽  
Thyroid Stimulating Hormone ◽  
Significant Inhibition ◽  
Male Rats ◽  
Prolactin Release ◽  
Medial Basal Hypothalamus ◽  
Hypophysectomized Rats ◽  
Adrenalectomized Rats ◽  
Intact Rats

The possible direct effect of corticosterone on release of pituitary prolactin was examined in a system using incubation for 8 h. Corticosterone at either 0·1 or 1 μg/ml medium had no significant effect on in-vitro prolactin release but 10 or 100 μg/ml medium produced a significant inhibition of release of prolactin. Release of LH, FSH and thyroid-stimulating hormone were not altered by 0·1, 1 or 10 μg corticosterone/ml, indicating that its action at the concentration of 10 μg/ml was specific on release of prolactin. Corticosterone injected at doses of 1 or 5 mg/kg into hypophysectomized rats with two pituitary grafts underneath the kidney capsule produced a significant fall in serum levels of prolactin when compared with control hypophysectomized rats with two pituitary grafts. Examination with the electron microscope showed that about one third of the lactotrophes from adrenalectomized rats after corticosterone injection exhibited patterns which suggested a decrease in protein synthesis when compared with lactotrophes from adrenalectomized rats given only the vehicle injection. These observations indicated that inhibition of release of prolactin by corticosterone could be exerted directly on the pituitary gland, and that the rise of serum levels of prolactin after adrenalectomy might have been due to the removal of direct inhibition by corticosterone. Male rats were adrenalectomized and 2–3 weeks later, concentrations of dopamine and noradrenaline in the medial basal hypothalamus were measured and found not to be different from values in intact rats. Dopamine metabolism also was not altered in the median eminence. The dopaminergic agonist, l-DOPA, inhibited, and the antagonists, pimozide and haloperidol, stimulated release of prolactin in both adrenalectomized and intact rats. Serotonin (5-HT) metabolism in the medial basal hypothalamus and anterior hypothalamus of adrenalectomized rats was not significantly different from values in intact rats, but a higher concentration of 5-HT was observed in the medial basal hypothalamus of adrenalectomized rats when compared with the values in intact rats. A serotonergic agonist, fluoxetine, and an antagonist, cyproheptadine, had no apparent effect on release of prolactin in intact rats, but fluoxetine produced a significant rise, and cyproheptadine, a significant lowering of serum levels of prolactin in adrenalectomized rats. These results suggest that 5-HT, but not dopamine, may be involved in the rise of prolactin after adrenalectomy.

Hypothalamus-pituitary-thyroid axis interactions with pineal gland in the rat.

1979 ◽  
Vol 236 (4) ◽  
pp. E416 ◽  
Author(s):  
G L Brammer ◽  
J E Morley ◽  
E Geller ◽  
A Yuwiler ◽  
J M Hershman
Keyword(s):  
Pineal Gland ◽  
Serum Levels ◽  
Thyroid Stimulating Hormone ◽  
Free Triiodothyronine ◽  
Prolactin Release ◽  
Free Thyroxine Index ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Melatonin Production

We examined in the rat several possible relationships between the pineal gland and the hypothalamus-pituitary-thyroid axis. The pineal gland, the retina, and the hypothalamus exhibited a diurnal rhythm in thyrotropin-releasing hormone (TRH) content with peak values occurring around 1200 h. This rhythm in the hypothalamus was abolished by constant light but was not affected by pinealectomy. Nor did pinealectomy affect hypothalamic TRH content, pituitary content of thyroid-stimulating hormone (TSH) or prolactin; serum levels of (TSH), triiodothyronine (T3), or thyroxine (T4), or serum free-thyroxine index; or free-triiodothyronine index. Melatonin did not affect TSH or prolactin release from the anterior pituitary or TRH release from the hypothalamus in vitro. Isoproterenol did not affect the TRH content of pineal glands in vitro; nor did TRH or T3 affect basal or stimulated activities of serotonin N-acetyltransferase, the presumed controlling enzyme in melatonin production. We found no evidence for significant interactions between the pineal gland and the hypothalamus-pituitary-thyroid axis.

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

Is aldosterone synthesized within the rat brain?

2005 ◽  
Vol 288 (2) ◽  
pp. E342-E346 ◽  
Author(s):  
Elise P. Gomez-Sanchez ◽  
Naveed Ahmad ◽  
Damian G. Romero ◽  
Celso E. Gomez-Sanchez
Keyword(s):  
De Novo ◽  
High Salt Diet ◽  
Salt Diet ◽  
Aldosterone Production ◽  
Paracrine Activation ◽  
Sodium Replacement ◽  
The Brain ◽  
Adrenalectomized Rats ◽  
Intact Rats

Very small amounts of adrenocorticosteroids are synthesized by brain tissue in vitro. While there is evidence suggesting that the synthesis of aldosterone in the brain may have a role in the hypertension of the Dahl salt-sensitive rat, the de novo synthesis of aldosterone or corticosterone within the brain of a living animal has not been demonstrated. We have used sensitive ELISAs to measure aldosterone and corticosterone in the plasma and whole brains of intact rats receiving a normal-, low-, or high-salt diet to alter adrenal aldosterone production and of adrenalectomized rats provided sodium replacement, some of which received aldosterone, corticosterone, or DOC replacement. The results of several experiments were consistent. In intact rats, the brain concentration of aldosterone and corticosterone reflected that in the plasma. However, whereas aldosterone and corticosterone were undetectable or barely undetectable in the plasma of adrenalectomized animals, as was the corticosterone in their brains, aldosterone was consistently found in the brains of adrenalectomized rats, ranging from a mean of 6.6–41 pg/g, depending on the experiment. Provision of DOC as substrate for the endogenous aldosterone synthase and 11β-hydroxylase did not significantly increase brain aldosterone or corticosterone content. It is postulated that the small amounts of aldosterone synthesized in the brain could provide a local ligand for autocrine or paracrine activation of the mineralocorticoid receptor.

THE ROLE OF THE ADRENAL GLAND IN THE CONTROL OF AMINO ACID INCORPORATION INTO PROTEIN OF ISOLATED RAT LIVER MICROSOMES

1960 ◽  
Vol 21 (2) ◽  
pp. 177-189 ◽  
Author(s):  
A. KORNER
Keyword(s):  
Amino Acid ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Female Rats ◽  
Male Rats ◽  
Rat Liver Microsomes ◽  
Hypophysectomized Rats ◽  
Normal Rat ◽  
Secondary Result

SUMMARY 1. Microsomes, isolated from rat liver a day after adrenalectomy, incorporate more radioactive amino acid into their protein in vitro than microsomes from normal rat liver. This enhanced rate of incorporation progressively declines with time after adrenalectomy until it reaches a plateau level which is below the normal rate of incorporation. 2. Following adrenalectomy microsomes isolated from liver of male rats show a greater rise in incorporating ability than those from liver of female rats, and maintain it longer. 3. Most of the increased incorporation observed in the in vitro system soon after adrenalectomy of the rat, and most of the decreased incorporation observed in rats adrenalectomized for some time, results from alterations in the microsomes which change their ability to incorporate activated amino acids into proteins. 4. Treatment of rats with cortisol acetate results in an increase in the ability of liver microsomes to incorporate amino acid into protein. This heightened incorporating ability is probably a secondary result of the breakdown of extrahepatic tissue protein which is stimulated by cortisol. 5. Somewhat similar responses to acute adrenalectomy and to treatment with cortisol were found in hypophysectomized rats. 6. The protein anabolic response of adrenalectomized rats to treatment with insulin, and of adrenalectomized-hypophysectomized rats to treatment with insulin or growth hormone, is greater than that shown by rats which possess adrenal glands.

scholarly journals Influence of Several Hormones on Erythropoiesis and Oxygen Consumption in the Hypophysectomized Rat

Blood ◽  
1962 ◽  
Vol 19 (5) ◽  
pp. 557-565 ◽  
Author(s):  
JAMES W. FISHER ◽  
JERRY J. CROOK
Keyword(s):  
Oxygen Consumption ◽  
Cell Volume ◽  
Thyroid Stimulating Hormone ◽  
Red Cell ◽  
Adrenocorticotrophic Hormone ◽  
Red Cell Volume ◽  
Iron Incorporation ◽  
Hypophysectomized Rats ◽  
Adrenalectomized Rats ◽  
Stimulating Hormone

Abstract Adrenocorticotrophic hormone (ACTH), thyroid stimulating hormone (TSH), adrenocortical extract (ACE), hydrocortisone (F), corticosterone (B), 11-dehydrocorticosterone and 3,5,3'-triiodothyronine (T-3) induced a moderate to marked erythropoietic effect in the hypophysectomized rat as indicated by an increase in both Fe59 incorporation in RBC and total circulating red cell volume. A corresponding increase in oxygen consumption was also observed. Angiotensin increased red cell volume and radioactive iron incorporation in RBC of hypophysectomized rats and stimulated Fe59 incorporation in hypophysectomized-adrenalectomized rats, but did not exert a significant effect on oxygen consumption. Cobalt injections resulted in a significant increase in red cell volume and Fe59 incorporation in RBC of hypophysectomized rats, but produced a significant decrease in oxygen consumption. The significance of these findings is discussed.

scholarly journals OBSERVATIONS ON THE INFLUENCE OF THE HYPOPHYSIS AND THE ADRENAL CORTEX ON BLOOD PLATELET LEVELS

Blood ◽  
1949 ◽  
Vol 4 (8) ◽  
pp. 936-946 ◽  
Author(s):  
ELIJAH ADAMS
Keyword(s):  
Bone Marrow ◽  
Adrenal Cortex ◽  
Blood Platelets ◽  
Blood Platelet ◽  
Distilled Water ◽  
Hypophysectomized Rats ◽  
Physiologic Saline ◽  
Maximum Rise ◽  
Adrenalectomized Rats ◽  
Intact Rats

Abstract Observations were made to investigate possible endocrine influences on blood platelets. Adrenal cortex extract failed to influence the platelet counts of mice, rats, or rabbits. Adrenalectomy and sham-adrenalectomy were followed by almost identical platelet increases in mice and rats. Administration of adrenal cortex extract, or physiologic saline, to adrenalectomized rats was followed by a consistent fall in platelets not observed in sham-adrenalectomized rats, or after administering distilled water to adrenalectomized rats. Platelet levels in hypophysectomized rats were significantly lower than in unoperated controls. Splenectomy in hypophysectomized rats was followed by a maximum rise in platelets markedly lower than following splenectomy in intact rats. Bone-marrow megakaryocytes in hypophysectomized rats were significantly fewer than in intact rats. No changes in megakaryocyte number or morphology appeared following splenectomy either in intact or hypophysectomized rats.

Adrenocorticotropic activity in the rat assessed by in vivo and in vitro indices

1963 ◽  
Vol 205 (6) ◽  
pp. 1083-1088 ◽  
Author(s):  
J. J. Van Goch ◽  
D. De Wied ◽  
E. Schönbaum
Keyword(s):  
Ascorbic Acid ◽  
Plasma Corticosterone ◽  
In Vitro Technique ◽  
Rat Adrenals ◽  
Hypophysectomized Rats ◽  
Adrenal Corticosterone ◽  
Intact Rats

Several indices of adrenocorticotropic (ACTH) activity were compared in order to establish the index most suitable for assay purposes, particularly of ACTH in blood. In hypophysectomized rats, the effects of ACTH on adrenal ascorbic acid, cholesterol, and steroid formation in vitro were studied. In intact rats, the effects of formalin on these variables as well as on the adrenal and plasma corticosterone levels and hypophyseal and blood ACTH activity were measured. Adrenal corticosterone as well as steroid formation in vitro increased very rapidly after stimulation by ACTH. In hypophysectomized rats, after intravenous ACTH, significant increases were observed after 5 min. In normal rats, 3 min after the injection of formalin, significant increases of steroid formation in vitro and ACTH activity were observed. The in vitro technique is suitable for the study of changes in ACTH activity. ACTH increases the fraction of corticosterone found in the total amount of corticoid secreted by rat adrenals in vitro.

THE COMBINED EFFECT OF MONOAMINE OXIDASE INHIBITORS AND CORTICOSTEROIDS ON THE PITUITARY-GONADAL SYSTEM OF MALE RATS

1966 ◽  
Vol 35 (3) ◽  
pp. 217-222 ◽  
Author(s):  
U. ZOR ◽  
H. AILABOUNI ◽  
F. G. SULMAN
Keyword(s):  
Monoamine Oxidase ◽  
Combined Treatment ◽  
Prostate Gland ◽  
Thyroid Stimulating Hormone ◽  
Monoamine Oxidase Inhibitors ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Accessory Sex Glands ◽  
Somatotrophic Hormone ◽  
Intact Rats

SUMMARY The mechanism by which combined treatment with monoamine oxidase inhibitors and a corticosteroid reduces the weight of the accessory sex glands in intact rats by about one half has been studied. Phenelzine sulphate in combination with hydrocortisone acetate given for 30 days to ovariectomized rats reduced the pituitary stores of luteinizing hormone (LH) by 33%. Similar reductions in somatotrophic hormone, corticotrophin and thyroid-stimulating hormone content were found after comparable treatment, whereas luteotrophic hormone increased. The increase of weight of the seminal vesicles and prostate gland produced by human chorionic gonadotrophin could be partly antagonized by the simultaneous administration of mebanazine and dexamethasone, but the action of testosterone on these glands in castrated animals was not inhibited. Interference with the production and effectiveness of LH is therefore the most likely mode of action by which these drugs effect the reduction of the weight of the accessory sex glands.

INFLUENCE OF THE ANTERIOR PITUITARY ON THE ALDOSTERONE SECRETORY RESPONSE TO DIETARY SODIUM RESTRICTION IN THE RAT

1968 ◽  
Vol 42 (3) ◽  
pp. 465-475 ◽  
Author(s):  
T. C. LEE ◽  
B. van der WAL ◽  
D. de WIED
Keyword(s):  
Anterior Pituitary ◽  
Normal Diet ◽  
Dietary Sodium ◽  
Sodium Restriction ◽  
Aldosterone Production ◽  
Hypophysectomized Rats ◽  
Dietary Sodium Restriction ◽  
Long Acting ◽  
Intact Rats

SUMMARY Studies of the rate of aldosterone production in vitro of adrenals of rats hypophysectomized before dietary sodium restriction showed that hypophysectomy not only prevented the increases in aldosterone production observed in intact, Na-deprived rats, but also depressed the level of aldosterone production to below that of intact rats maintained on a normal diet. Rats hypophysectomized for a similar period of time but maintained on the normal diet showed a similar decrease. Experiments on adeno- and neuro-hypophysectomized rats indicated that the pituitary factor required for the normal mineralocorticoid response to dietary sodium restriction resides in the anterior pituitary. Treatment of hypophysectomized rats during dietary sodium restriction with doses of a long-acting corticotrophin (ACTH) prevented adrenal atrophy and maintained a normal glucocorticoid response to intravenous injections of ACTH, but failed to increase aldosterone production rates in vitro to levels above that of intact rats on a normal diet; it also failed to restore the enhanced adrenocortical sensitivity to the stimulating effect of aldosterone production of intravenously injected ACTH which is characteristic of acutely hypophysectomized, Na-deficient rats. Treatment with anterior pituitary powder (8–12 mg./day) for similar periods, however, restored the aldosterone production of adrenals in vitro of hypophysectomized, Na-deprived rats to levels nearly indistinguishable from those of acutely hypophysectomized, Na-deprived controls. The same doses of anterior pituitary powder were shown not to have any demonstrable effect on the aldosterone production of adrenals in vitro of intact rats on a normal diet. These results are interpreted as indicating the existence of a pituitary factor other than ACTH which stimulates aldosterone secretion. This factor does not appear to act directly on the adrenal cortex or to stimulate the secretion of specific glomerulotropic substances, but probably exerts its effect by maintaining the normal functional capacity of some as yet undefined tissues which secrete glomerulotropic substances in response to dietary sodium restriction.

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.

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