PARATHYROID HORMONE AND PHOSPHATE HOMEOSTASIS IN MAN

1964 ◽  
Vol 46 (2) ◽  
pp. 285-291 ◽  
Author(s):  
Allan Halden ◽  
E. Eisenberg ◽  
Gilbert S. Gordan
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Phosphorus Loading ◽  
Phosphate Homeostasis ◽  
Renal Handling ◽  
Tubular Resorption ◽  
Renal Tubular ◽  
Renal Responses ◽  
Urine And Serum ◽  
Phosphorus Intake

ABSTRACT To determine whether parathyroid hormone is required for renal response to phosphorus loading, the effects of ingestion of 3100 mg of phosphorus daily for 3 days were compared in 5 treated hypoparathyroid patients and 5 normal control subjects of comparable age and sex. In both normal and hypoparathyroid subjects the response to phosphorus loading was characterized by an increase in urinary excretion of phosphorus without a concomitant increase in the rate of glomerular filtration of phosphorus. Some mechanism other than changes in rates of parathyroid hormone secretion probably accounts for renal responses to changes in phosphorus intake. The timing of urine and serum collections with regard to food intake and the total amount of phosphorus in the diet were found to affect the assessment of renal handling of phosphorus. The finding that a 3-day period of oral phosphorus loading did not increase the serum phosphorus level in the hypoparathyroid patients suggests that phosphorus restriction is not always necessary in the treatment of hypoparathyroidism. The addition of one more condition to the list of those that may affect the percentage of renal tubular resorption of phosphorus in no way decreases the usefulness of this determination in the diagnosis of hyperparathyroidism.

PARATHYROID FUNCTION IN SPONTANEOUS PRIMARY HYPOTHYROIDISM

1968 ◽  
Vol 40 (4) ◽  
pp. 467-475 ◽  
Author(s):  
P. ADAMS ◽  
T. M. CHALMERS ◽  
B. L. RIGGS ◽  
J. D. JONES
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Primary Hypothyroidism ◽  
Tubular Reabsorption ◽  
Target Cells ◽  
Serum Calcium Concentration ◽  
Parathyroid Function ◽  
Renal Tubular Reabsorption ◽  
The Mean ◽  
Renal Tubular

SUMMARY Calcium and phosphorus metabolism were studied in 22 patients with spontaneous primary hypothyroidism. Two patients were found to have hypercalcaemia but the mean serum calcium concentration of the group was significantly less than that of control subjects. The renal tubular reabsorption of phosphate was decreased and could be increased to normal with small calcium infusions. The response to calcium deprivation and to infusions of EDTA was abnormal and suggested an impaired ability to mobilize calcium from bone. There was a significant correlation between the defect in calcium mobilization, as judged from the response to EDTA, and the renal tubular reabsorption of phosphate. In three patients serum parathyroid hormone concentrations, measured by radioimmunoassay, were in the upper part of the normal range. It is suggested that in patients with hypothyroidism the target cells in bone are less responsive to the effects of parathyroid hormone than normal; as a consequence parathyroid hormone secretion may be increased.

Self-limited Neonatal Familial Hyperparathyroidism Associated With Hypercalciuria and Renal Tubular Acidosis in Three Siblings

PEDIATRICS ◽  
1990 ◽  
Vol 86 (3) ◽  
pp. 421-427
Author(s):  
Soroku Nishiyama ◽  
Shinichi Tomoeda ◽  
Fumitaka Inoue ◽  
Takao Ohta ◽  
Ichiro Matsuda
Keyword(s):  
Parathyroid Hormone ◽  
Serum Calcium ◽  
Renal Tubular Acidosis ◽  
Autosomal Recessive ◽  
Hormone Secretion ◽  
Autosomal Recessive Inheritance ◽  
Serum Parathyroid Hormone ◽  
Calcium Loading ◽  
Renal Tubular ◽  
Familial Hyperparathyroidism

Three siblings with neonatal familial hyperparathyroidism diagnosed at age 4 months, 2 months, and 5 days, respectively, were treated. Hypercalciuria, nephrocalcinosis, and renal tubular acidosis were present in each child. In all three, there were higher responses of serum parathyroid hormone to serum calcium and higher elevation of serum calcium with oral calcium loading. The metabolism of vitamin D and calcitonin seemed to be intact. Hypercalcemia associated with the abnormal response of parathyroid hormone secretion disappeared when the children passed the age of approximately 2 years, although renal tubular acidosis and nephrocalcinosis remained. An autosomal recessive inheritance seems likely.

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

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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