Regulation of parathyroid hormone secretion in vitro and in vivo

1982 ◽  
Vol 34 (1) ◽  
pp. 313-316 ◽  
Author(s):  
J. A. Fischer ◽  
J. W. Blum ◽  
W. Born ◽  
M. A. Dambacher ◽  
D. W. Dempster
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion

Prolactin stimulation of parathyroid hormone secretion in bovine parathyroid cells

1984 ◽  
Vol 247 (5) ◽  
pp. E675-E680 ◽  
Author(s):  
L. Magliola ◽  
L. R. Forte
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Vitamin D Metabolism ◽  
Parathyroid Function ◽  
Wide Range ◽  
Camp Levels ◽  
Bovine Species ◽  
Ca Homeostasis

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.

scholarly journals Fluoride Modulates Parathyroid Hormone Secretion in vivo and in vitro

2015 ◽  
Vol 200 (6) ◽  
pp. 413-423 ◽  
Author(s):  
Chaitanya P. Puranik ◽  
Kathleen A. Ryan ◽  
Zhaoyu Yin ◽  
E. Angeles Martinez-Mier ◽  
John S. Preisser ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion

scholarly journals Suppression of parathyroid hormone production in vitro and in vivo by RNA interference

2009 ◽  
Vol 75 (5) ◽  
pp. 490-498 ◽  
Author(s):  
Genta Kanai ◽  
Takatoshi Kakuta ◽  
Kaichiro Sawada ◽  
Tun A. Yokoyama ◽  
Reika Tanaka ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Rna Interference ◽  
Hormone Production

Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær
Keyword(s):  
Arginine Vasopressin ◽  
Mode Of Action ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Pituitary Hormones ◽  
Pituitary Hormone ◽  
Anterior Pituitary Hormones ◽  
Anterior Pituitary Hormone

Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1− and V2−receptors, where the pituitary V1−receptor is designated V1b. The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1− receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V1b− receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1− receptors) as well as permissive (utilizing mainly V1− but also V2−receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1−receptors but V2−receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1 −receptors) and permissive (utilizing both V1− and V2− receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.

scholarly journals Intercellular communication in the rat anterior pituitary gland: an in vivo and in vitro study

1975 ◽  
Vol 67 (2) ◽  
pp. 469-476 ◽  
Author(s):  
WH Fletcher ◽  
NC Anderson ◽  
JW Everett
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
In Vitro Study ◽  
Anterior Pituitary Gland ◽  
Stimulus Secretion Coupling ◽  
Unpublished Observation ◽  
Cellular Ca

The concept of "stimulus-secretion coupling" suggested by Douglas and co-workers to explain the events related to monamine discharge by the adrenal medulla (5, 7) may be applied to other endocrine tissues, such as adrenal cortex (36), pancreatic islets (4), and magnocellular hypothalamic neurons (6), which exhibit a similar ion-dependent process of hormone elaboration. In addition, they share another feature, that of joining neighbor cells via membrane junctions (12, 26, and Fletcher, unpublished observation). Given this, and the reports that hormone secretion by the pars distalis also involves a secretagogue-induced decrease in membrane bioelectric potential accompanied by a rise in cellular [Ca++] (27, 34, 41), it was appropriate to test the possibility that cells of the anterior pituitary gland are united by junctions.

Comparison of the feedback effect of magnesium and calcium on parathyroid hormone secretion in man

1987 ◽  
Vol 113 (1) ◽  
pp. 117-122 ◽  
Author(s):  
O. Ferment ◽  
P. E. Garnier ◽  
Y. Touitou
Keyword(s):  
Parathyroid Hormone ◽  
Urinary Excretion ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Magnesium Salt ◽  
Saline Injection ◽  
Molar Basis ◽  
Magnesium Salts ◽  
High Doses

ABSTRACT Administration of high doses of magnesium is known to produce a decrease in parathyroid hormone (PTH) secretion in human patients but the effect of magnesium on the secretion of PTH in healthy man is not known. We have looked at the effect of a relatively moderate i.v. dose of magnesium (7·08 mmol) in seven healthy men. In addition and for comparison the effect of calcium (4·25 mmol) was studied. Two magnesium salts were considered, magnesium sulphate (MgSO4) and magnesium pyrrolidone carboxylate (MgPC). Four i.v. injections were given at 08.00 h (MgPC, NaCl (control), MgSO4 and Ca gluconate), with an interval of 1 week between each injection. Whatever the magnesium salt the variations in plasma concentrations of magnesium were the same whereas no change in erythrocyte magnesium was observed. Plasma concentration of C-terminal PTH did not show significant variations after MgPC or saline injection. Both MgSO4 and Ca gluconate produced a statistically significant 30% decrease in plasma PTH levels 45 min after the injection. The effect was more sustained with calcium (2 h) than with magnesium (45 min). The urinary excretion of magnesium was significantly higher after injection of MgSO4 than after MgPC. These results suggest (1) that magnesium was, on a molar basis, less potent than calcium in regulating PTH secretion in vivo, (2) that the nature of the magnesium salt used must be kept in mind for the interpretation of the effect of magnesium on PTH secretion in vivo and (3) that the decrease in plasma PTH can partly explain the larger urinary excretion of magnesium after MgSO4 than after MgPC. J. Endocr. (1987) 113, 117–122

In vivo effects of flavonoid EMD 21388 on thyroid hormone secretion and metabolism in rats

1991 ◽  
Vol 261 (2) ◽  
pp. E227-E232 ◽  
Author(s):  
J. P. Schroder-van der Elst ◽  
D. van der Heide ◽  
J. Kohrle
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Male Rats ◽  
Intact Male ◽  
Hormone Production ◽  
Iodide Uptake ◽  
Brown Adipose ◽  
In Vivo Effects

In vitro, the synthetic flavonoid EMD 21388 appears to be a potent inhibitor of thyroxine (T4) 5'-deiodinase and diminishes binding of T4 to transthyretin. In this study, in vivo effects of long-term administration of EMD 21388 on thyroid hormone production and metabolism were investigated. Intact male rats received EMD 21388 (20 mumol.kg body wt-1.rat-1.day-1) for 14 days. [125I]T4 and 3,5,3'-[131I]triiodotyronine (T3) were infused continuously and intravenously in a double-isotope protocol for the last 10 and 7 days, respectively. EMD 21388 decreased plasma thyroid hormone concentrations, but thyrotropin levels in plasma and pituitary did not change. Plasma clearance rates for T4 and T3 increased. Thyroidal T4 secretion was diminished, but T3 secretion was elevated. Extrathyroidal T3 production by 5'-deiodination was lower. T4 concentrations were markedly lower in all tissues investigated. Total tissue T3 was lower in brown adipose tissue, brain, cerebellum, and pituitary, tissues that express the type II 5'-deiodinase isozyme due to decreased local T3 production. Most tissues showed increased tissue/plasma ratios for T4 and T3. These results indicate that this flavonoid diminished T4 and increased T3 secretion by the thyroid, probably in analogy with other natural flavonoids, by interference with one or several steps between iodide uptake, organification, and hormone synthesis.

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