Ca2+-Induced Increases in Steady-State Concentrations of Intracellular Calcium Are Not Required for Inhibition of Parathyroid Hormone Secretion

1999 ◽  
Vol 1 (3) ◽  
pp. 221-226 ◽  
Author(s):  
J. Russell ◽  
W. Zhao ◽  
G. Christ ◽  
S. Ashok ◽  
R.H. Angeletti
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Intracellular Calcium ◽  
Hormone Secretion

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.

scholarly journals 1,25(OH)2-vitamin D3 reduces spontaneous and hypocalcemia-stimulated pulsatile component of parathyroid hormone secretion.

1998 ◽  
Vol 9 (1) ◽  
pp. 54-62
Author(s):  
C P Schmitt ◽  
F Schaefer ◽  
D Huber ◽  
I Zahn ◽  
J D Veldhuis ◽  
...  
Keyword(s):  
Steady State ◽  
Parathyroid Hormone ◽  
Vitamin D3 ◽  
Hormone Secretion ◽  
Burst Frequency ◽  
Pulsatile Secretion ◽  
Deconvolution Technique ◽  
Before And After ◽  
Selective Increase ◽  
Secretory Capacity

To investigate the effects of 1,25(OH)2-vitamin D3 (1,25(OH)2D3) on pulsatile parathyroid hormone (PTH) release, minute-to-minute intact PTH secretion was examined in nine healthy adults under baseline conditions and during hypocalcemia (sodium citrate clamp) before and after 5 d of oral 1,25(OH)2D3 treatment (1 microgram/d). In addition, acute effects of 1,25(OH)2D3 were examined by a single intravenous bolus of 2 micrograms of 1,25(OH)2D3. Pulsatile and tonic PTH secretion rates were calculated by the multiparameter deconvolution technique. During baseline, 68% of circulating PTH was attributable to tonic, and 32% to pulsatile, secretion. During induction of hypocalcemia, a selective increase in pulsatile secretion (+1100%), mediated by a combined increase in burst frequency and burst mass, was observed. During the subsequent steady-state hypocalcemic period, burst frequency and mass decreased and tonic secretion increased to 3 times the baseline level. Intravenous 1,25(OH)2D3 did not affect the temporal pattern of PTH secretion. In contrast, oral 1,25(OH)2D3 decreased baseline plasma PTH by 30% without a detectable change in Ca2+. This suppression was accounted for mainly by a decrease in PTH burst frequency. During hypocalcemia induction, a significantly lower (30%) increase in burst mass occurred compared with the pretreatment study. During steady-state hypocalcemia, PTH burst mass (-45%) and pulsatile (-50%) and total (-35%) secretion rate were lower than before treatment. In conclusion, acute hypocalcemia selectively increases pulsatile PTH release by stimulating both burst frequency and mass via a Ca2+ rate-sensitive mechanism. Oral 1,25-(OH)2D3 suppresses pulsatile baseline PTH release and reduces the pulsatile secretory capacity of the parathyroids during a hypocalcemic stimulus.

PARATHYROID HORMONE SECRETION IN DISORDERS OF CALCIUM METABOLISM STUDIED BY MEANS OF EDTA

1974 ◽  
Vol 75 (2) ◽  
pp. 286-296 ◽  
Author(s):  
J. H. Lockefeer ◽  
W. H. L. Hackeng ◽  
J. C. Birkenhäger
Keyword(s):  
Parathyroid Hormone ◽  
Primary Hyperparathyroidism ◽  
Calcium Metabolism ◽  
Hormone Secretion ◽  
Parathyroid Tissue ◽  
Small Mass ◽  
Idiopathic Hypercalciuria ◽  
List Type ◽  
Immunoreactive Parathyroid Hormone ◽  
Pth Level

ABSTRACT In 22 of 28 cases of primary hyperparathyroidism (PHP) the rise in the serum immunoreactive parathyroid hormone (IRPTH or PTH) level observed in response to lowering of the serum calcium by EDTA, exceeded that obtained in 8 control subjects. In 5 of these 22 patients who were studied again after parathyroidectomy the supranormal response was abolished. Fifteen of these 22 hyper-responsive PHP patients had basal IRPTH levels not exceeding the highest level in the controls and that of other groups of patients investigated (idiopathic hypercalciuria, non-parathyroid hypercalcaemia, operated PHP). Fourteen of the 22 hyper-reactive patients with PHP did not show hypocalcaemia during the infusion of EDTA. The extent of the release of PTH elicited by EDTA in cases of PHP does not as yet allow a prediction of the amount of pathological parathyroid tissue present, although all the PHP patients showing a normal release of PTH had a relatively small mass of parathyroid tissue (up to about 1 g) subsequently removed. In 9 cases of nephrolithiasis (8 of whom had idiopathic hypercalciuria) and in 7 cases of non-parathyroid hypercalcaemia, a normal PTH release was found.

Pulse amplitude and frequency modulation of parathyroid hormone secretion in man

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S171 ◽  
Author(s):  
H. HARMS ◽  
U. KAPTAINA ◽  
T. KÜLPMANN ◽  
R.-D. HESCH
Keyword(s):  
Parathyroid Hormone ◽  
Frequency Modulation ◽  
Hormone Secretion ◽  
Pulse Amplitude ◽  
Amplitude And Frequency Modulation

scholarly journals Spontaneous oscillations of intracellular calcium and growth hormone secretion.

1988 ◽  
Vol 263 (20) ◽  
pp. 9682-9685
Author(s):  
R W Holl ◽  
M O Thorner ◽  
G L Mandell ◽  
J A Sullivan ◽  
Y N Sinha ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Intracellular Calcium ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Spontaneous Oscillations

Effect of phorbol myristate acetate on secretion of parathyroid hormone

1988 ◽  
Vol 254 (1) ◽  
pp. E63-E70 ◽  
Author(s):  
J. J. Morrissey
Keyword(s):  
Protein Kinase C ◽  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Membrane Fraction ◽  
Hormone Secretion ◽  
Myristate Acetate ◽  
Kinase C ◽  
Low Calcium ◽  
Protein Kinase C Activity ◽  
High Calcium

The influence of phorbol myristate acetate (PMA), an activator of protein kinase c, on the secretion of parathyroid hormone from collagenase-dispersed bovine parathyroid cells was tested. The cells were incubated at low (0.5 mM) or high (2.0 mM) concentrations of calcium in the medium, and the hormone secreted into the medium was measured by a radioimmunoassay that recognizes both intact and C-terminal fragments of hormone. At low calcium, the secretory rate averaged 32 +/- 3.8 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA did not affect secretion. At high calcium there was a significant suppression of secretion by 38% to 19.8 +/- 3 ng.h-1.(10(5) cells)-1. The addition of 1.6 microM PMA significantly stimulated hormone secretion to 35.8 +/- 8 ng.h-1.(10(5) cells)-1, a rate indistinguishable from low calcium. This stimulatory effect of PMA at high calcium was seen at PMA concentrations as low as 1.6 nM, did not occur with a biologically inactive 4 alpha-isomer of phorbol ester, and was independent of changes in cellular adenosine 3',5'-cyclic monophosphate levels. Examination of 32P-labeled phosphoproteins by two-dimensional gel electrophoresis revealed acidic proteins of approximately 20,000 and 100,000 Da that were phosphorylated at low and high calcium + 1.6 microM PMA but not at high calcium alone. The protein kinase c activity associated with the membrane fraction of parathyroid cells significantly decreased 40% when the cells were incubated at high vs. low calcium. The data suggest that calcium may regulate parathyroid hormone secretion through changes in protein kinase c activity of the membrane fraction of the cell and protein phosphorylation.

Parathyroid Hormone- and Deoxycorticosterone Acetate-Induced Hypertension in the Rat

1980 ◽  
Vol 58 (5) ◽  
pp. 365-371 ◽  
Author(s):  
A. Berthelot ◽  
A. Gairard
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Sprague Dawley ◽  
Physiological Concentration ◽  
Deoxycorticosterone Acetate ◽  
Calcium Diet ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
High Calcium ◽  
High Calcium Diet

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

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