Functional dedifferentiation of parathyroid cells results both from a defective regulation and action of cytoplasmic Ca2+

1986 ◽  
Vol 6 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Peter Nygren
Keyword(s):  
Parathyroid Hormone ◽  
Inhibitory Action ◽  
Monolayer Culture ◽  
Hormone Secretion ◽  
Dose Effect ◽  
Parathyroid Cell ◽  
Hormone Release ◽  
Parathyroid Adenomas ◽  
Small Inhibition

Monolayer culture of bovine parathyroid cells for 24 hours resulted in a right-shift of the dose-effect relationships for Ca2+-inhibition of parathyroid hormone (PTH) release and the dependence of the cytoplasmic Ca2+ concentration (Ca2+) on extracellular Ca2+ as well as in a less suppressible hormone release. After 4 days of culture, hormone secretion was almost non-suppressible and Cai2+ increased poorly in response to a rise in extracelluiar Ca2+. Ionomycin, a Ca2+ ionophore, raised Cai2+, but there was only a small inhibition of PTH release and the correlation between Cai2+ and secretion was weak. A deteriorated Cai2+ regulation and a decreased inhibitory action of cytoplasmic Ca2+ on PTH release were also found in ceils from human parathyroid adenomas. Functional dedifferentiation of the parathyroid cell thus results from both defective regulation and action of cytoplasmic Ca2+.

Regulation of acute parathyroid hormone release in normal humans: combined calcium and citrate clamp study

1992 ◽  
Vol 263 (2) ◽  
pp. E195-E198 ◽  
Author(s):  
P. Schwarz ◽  
H. A. Sorensen ◽  
I. Transbol ◽  
P. McNair
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Ionized Calcium ◽  
Intact Parathyroid Hormone ◽  
Hormone Release ◽  
Hormone Regulation ◽  
Clamp Technique ◽  
Baseline Concentration ◽  
Parathyroid Hormone Release

The objective of the present study was to elucidate the dynamics of parathyroid hormone regulation, with particular reference to the mechanism controlling the acute parathyroid hormone release. Through utilization of the citrate clamp technique and the calcium clamp technique we were able, in a standardized way, to stimulate and suppress the parathyroid hormone secretion. Precise bedside measurements of blood ionized calcium and measurements of intact parathyroid hormone were performed. Twelve healthy young volunteers participated in two trials 6-12 wk apart, a citrate clamp (delta-blood ionized calcium -0.19 mmol/l) and a calcium plus citrate clamp (delta-blood ionized calcium +0.22 mmol/l and -0.19 mmol/l). During the citrate clamp, preceded by normal calcemia, serum intact parathyroid hormone peaked to a maximum after 5-10 min, four to six times above baseline concentration and then declined to a steady state two to three times above baseline concentration. During the citrate clamp, preceded by hypercalcemia induced by a calcium clamp, serum intact parathyroid hormone also peaked immediately to about five to nine times above its suppressed level, approximately two times above the baseline concentration. Subsequently, serum intact parathyroid hormone declined to a steady state just below the baseline concentration. In conclusion, within the range studied, the mechanism eliciting the acute serum intact parathyroid hormone release from its depot is a fall in blood ionized calcium, not the absolute concentration of ionized calcium.

THE EFFECT OF CALCIUM AND DIBUTYRYL-cAMP ON THE SECRETION OF PARATHYROID HORMONE BY HUMAN PARATHYROID ADENOMAS IN ORGAN CULTURE

1977 ◽  
Vol 85 (3) ◽  
pp. 541-547 ◽  
Author(s):  
M. Dietel ◽  
G. Dorn ◽  
R. Montz ◽  
E. Altenähr
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Organ Culture ◽  
Inverse Relationship ◽  
Calcium Concentration ◽  
Culture Medium ◽  
Hormone Secretion ◽  
Dibutyryl Camp ◽  
Parathyroid Adenomas ◽  
Immunoreactive Parathyroid Hormone

ABSTRACT The effect of different calcium concentrations as well as dibutyryl-cyclic adenosine 3′,5′-monophosphate (DB-cAMP) on the secretion of parathyroid hormone by human parathyroid adenomas taken from patients with primary hyperparathyroidism (pHPT) was studied in organ culture. Their influence on the release of hormone was determined. The tissue was incubated in culture medium for 4 h; the medium was changed hourly and analyzed for immunoreactive parathyroid hormone (PTH) by radioimmunoassay. The hormone secretion showed an inverse relationship to different calcium concentrations in the medium and could be stimulated independently of the calcium concentration by adding DB-cAMP. These results suggest that the examined parathyroid adenomas are sensitive to physiological stimuli.

THE SEROTONIN RETAINING EFFECT OF LITHIUM IN THE RAT THYROID

1976 ◽  
Vol 82 (2) ◽  
pp. 530-534 ◽  
Author(s):  
H. Vejlsted ◽  
O. Korsgaard
Keyword(s):  
Thyroid Hormone ◽  
Inhibitory Action ◽  
Hormone Secretion ◽  
Serotonin Release ◽  
Hormone Release ◽  
Rat Thyroid ◽  
Stimulation Of

ABSTRACT The hypothesis of a lithium induced serotonin retention in the rat thyroid has been tested. It has been found that the thyroid in rats treated with lithium contains double the amount of serotonin compared with glands from untreated animals. The ability of TSH to stimulate serotonin release is inhibited by lithium. The ability of serotonin to stimulate thyroid hormone secretion in vitro is documented. The inhibitory action of lithium on both TSH and serotonin stimulation of hormone release is documented. The serotonin retaining effect of lithium as part of the goitrogenic effect of this ion is discussed.

Dissociation of membrane potential and hormone secretion in bovine parathyroid cells

1983 ◽  
Vol 245 (1) ◽  
pp. E102-E105
Author(s):  
J. J. Morrissey ◽  
S. Klahr
Keyword(s):  
Parathyroid Hormone ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Calcium Ion ◽  
Cell Function ◽  
Hormone Secretion ◽  
Ion Concentration ◽  
Parathyroid Cell ◽  
High Potassium ◽  
Calcium Ion Concentration

An increase in the calcium ion concentration of the medium from 0.5 to 2.0 mM is associated with a 65% decrease in the secretion of parathyroid hormone from dispersed parathyroid cells. This maneuver also depolarized the cell membrane from -55 to -21 mV as measured by the distribution of [3H]tetraphenylphosphonium ion between cells and medium. An increase in the potassium ion concentration of the medium to 50 mM caused a 67% increase in hormone secretion at 0.5 mM calcium and depolarized the cell to -31 mV. The high potassium did not significantly change hormone secretion or the membrane potential at 2.0 mM calcium. Chlorpromazine inhibited hormone secretion by 40% and depolarized the cell to -30 mV at 0.5 mM calcium in the medium. Chlorpromazine did not change hormone secretion or membrane potential in cells incubated at 2.0 mM calcium. These results suggest that depolarization of the cell by calcium cannot account by itself for the inhibition of hormone secretion and chlorpromazine mimics the effect of an increase in calcium on parathyroid cell function.

Dopamine-stimulated parathyroid hormone release in vitro: further evidence for a two-pool model of parathyroid hormone secretion

1985 ◽  
Vol 63 (9) ◽  
pp. 1139-1144 ◽  
Author(s):  
David A. Hanley ◽  
Paul G. Wellings
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Hormone Release ◽  
Low Calcium ◽  
Pool Model ◽  
Parathyroid Hormone Release ◽  
Perifusion System ◽  
Sustained Increase

Bovine parathyroid tissue was placed in an in vitro perifusion system for the study of parathyroid hormone secretion stimulated by low calcium and dopamine. Dopamine caused a transient increase in parathyroid hormone release, while low calcium caused a sustained increase in parathyroid hormone secretion. The dopamine response was similar to that caused by isoproterenol. After parathyroid hormone release had been stimulated by dopamine there was no response to isoproterenol, suggesting they cause the release of the same cellular pool of hormone. Inhibition of protein synthesis with cycloheximide eliminated the response to low calcium, with no effect on dopamine-stimulated parathyroid hormone release. These studies suggest dopamine stimulates the release of a limited quantity storage pool of parathyroid hormone, while low calcium causes a sustained release of hormone by stimulating secretion of newly synthesized hormone. Low calcium has little or no effect on release of the storage granule pool of parathyroid hormone.

Parathyroid cell surface autoantibodies that inhibit parathyroid hormone secretion from dispersed human parathyroid cells

2009 ◽  
Vol 1 (5) ◽  
pp. 475-483 ◽  
Author(s):  
James T. Posillico ◽  
Jacobo Wortsman ◽  
Sath Srikanta ◽  
George S. Eisenbarth ◽  
Lawrence E. Mallette ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Cell Surface ◽  
Hormone Secretion ◽  
Parathyroid Cell

THE EFFECT OF 1,25-DIHYDROXYCHOLECALCIFEROL ON THE PARATHYROID HORMONE SECRETION OF PORCINE PARATHYROID GLANDS AND HUMAN PARATHYROID ADENOMAS IN VITRO

1977 ◽  
Vol 86 (3) ◽  
pp. 533-538 ◽  
Author(s):  
E. Altenähr ◽  
M. Dietel ◽  
G. Dorn ◽  
R. Montz
Keyword(s):  
Parathyroid Hormone ◽  
Parathyroid Adenoma ◽  
Hormone Secretion ◽  
Parathyroid Glands ◽  
Parathyroid Adenomas ◽  
Feedback Inhibitor ◽  
Adenoma Tissue ◽  
Parathyroid Hormone Release ◽  
Immunoreactive Parathyroid Hormone

ABSTRACT The effect of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) on parathyroid hormone secretion by porcine parathyroid glands and human parathyroid adenoma tissue was investigated by in vitro incubation. The addition of 100 nmoles 1,25-(OH)2-D3 to the medium inhibited significantly the release of immunoreactive parathyroid hormone by 63–65 %. This suppression was reversible when 1.25-(OH)2-D3 was removed again. The inhibition of parathyroid hormone release observed in human parathyroid adenoma tissue was similar to that in normal porcine parathyroid glands. This indicates that adenoma tissue is sensitive to regulatory influences. As well as calcium, 1,25-(OH)2-D3 may act as another feedback inhibitor of parathyroid hormone secretion.

Ga3+ inhibits parathyroid hormone release without interacting with the Ca2+ receptor of the parathyroid cell

1992 ◽  
Vol 186 (1) ◽  
pp. 556-561 ◽  
Author(s):  
Peter Ridefelt ◽  
Per Hellman ◽  
Osten Ljunggren ◽  
Sverker Ljunghall ◽  
Göran Åkerström ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Parathyroid Cell ◽  
Hormone Release ◽  
Parathyroid Hormone Release
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