scholarly journals Parathyroid hormone secretion in low calcium intake smokers

2001 ◽  
Vol 86 (2) ◽  
pp. 307-307
Author(s):  
D. Bonofiglio ◽  
S. Catalano ◽  
M. Maggiolini ◽  
S. Andò
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Intake ◽  
Hormone Secretion ◽  
Low Calcium

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.

scholarly journals Relation Between Low Calcium Intake, Parathyroid Hormone, and Blood Pressure

Hypertension ◽  
2000 ◽  
Vol 35 (5) ◽  
pp. 1154-1159 ◽  
Author(s):  
Rolf Jorde ◽  
Johan Sundsfjord ◽  
Egil Haug ◽  
Kaare H. Bønaa
Keyword(s):  
Blood Pressure ◽  
Parathyroid Hormone ◽  
Calcium Intake ◽  
Low Calcium

scholarly journals Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration

2013 ◽  
Vol 29 (2) ◽  
pp. 282-289 ◽  
Author(s):  
M. E. Rodriguez-Ortiz ◽  
A. Canalejo ◽  
C. Herencia ◽  
J. M. Martinez-Moreno ◽  
A. Peralta-Ramirez ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Calcium Concentration ◽  
Hormone Secretion ◽  
Receptor Expression ◽  
Low Calcium

scholarly journals Mechanisms Involved in the Relationship between Low Calcium Intake and High Blood Pressure

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1112 ◽  
Author(s):  
Cecilia Villa-Etchegoyen ◽  
Mercedes Lombarte ◽  
Natalia Matamoros ◽  
José M. Belizán ◽  
Gabriela Cormick
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Parathyroid Hormone ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Vascular Smooth Muscle Cells ◽  
Calcium Intake ◽  
Low Calcium Diet ◽  
Low Calcium

There is increasing epidemiologic and animal evidence that a low calcium diet increases blood pressure. The aim of this review is to compile the information on the link between low calcium intake and blood pressure. Calcium intake may regulate blood pressure by modifying intracellular calcium in vascular smooth muscle cells and by varying vascular volume through the renin–angiotensin–aldosterone system. Low calcium intake produces a rise of parathyroid gland activity. The parathyroid hormone increases intracellular calcium in vascular smooth muscles resulting in vasoconstriction. Parathyroidectomized animals did not show an increase in blood pressure when fed a low calcium diet as did sham-operated animals. Low calcium intake also increases the synthesis of calcitriol in a direct manner or mediated by parathyroid hormone (PTH). Calcitriol increases intracellular calcium in vascular smooth muscle cells. Both low calcium intake and PTH may stimulate renin release and consequently angiotensin II and aldosterone synthesis. We are willing with this review to promote discussions and contributions to achieve a better understanding of these mechanisms, and if required, the design of future studies.

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.

scholarly journals Association of bone microarchitecture with parathyroid hormone concentration and calcium intake in men: the STRAMBO study

2011 ◽  
Vol 165 (1) ◽  
pp. 151-159 ◽  
Author(s):  
A Chaitou ◽  
S Boutroy ◽  
N Vilayphiou ◽  
A Varennes ◽  
M Richard ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Bone Turnover ◽  
Calcium Intake ◽  
Bone Microarchitecture ◽  
Quantitative Computed Tomography ◽  
Distal Tibia ◽  
Volumetric Bone Mineral Density ◽  
Mineral Density ◽  
Low Calcium

ObjectiveIn the elderly, vitamin D deficit, low calcium intake, and impaired bone microarchitecture are associated with higher risk of hip fracture. We assessed the association of bone microarchitecture with calcium intake and serum concentrations of 25-hydroxycholecalciferol (25OHD) and parathyroid hormone (PTH) in men.DesignCross-sectional analysis was performed in 1064 men aged 20–87 years not taking vitamin D or calcium supplements.MethodsDaily calcium intake was assessed using a food frequency questionnaire. Bone microarchitecture was assessed at distal radius and tibia by high-resolution peripheral quantitative computed tomography. We measured serum and urinary levels of biochemical bone turnover markers (BTMs). Statistical models were adjusted for age, weight, height, and glomerular filtration rate.ResultsIn 500 men aged <65 years, lower 25OHD levels and low calcium intake were associated with lower trabecular volumetric bone mineral density (Dtrab) at the distal tibia, due to lower trabecular number (Tb.N). Low calcium intake was associated with lower cortical thickness (Ct.Th). Higher PTH level was associated with higher BTM levels. In 563 men aged ≥65 years, the highest PTH quartile was associated with lower Ct.Th (tibia), lower Dtrab (both sites), and lower Tb.N (radius) compared with the lowest quartile. Low calcium intake was associated with lower Tb.N and more heterogenous trabecular distribution. BTM positively correlated with the PTH concentration.ConclusionIn older men, elevated PTH concentration is associated with high bone turnover, poor trabecular microarchitecture (radius and tibia), and, at the distal tibia, lower Ct.Th. Low calcium intake is associated with lower Tb.N and more heterogenous trabecular distribution.

Effects of Mineral Composition of Drinking Water on Risk for Stone Formation and Bone Metabolism in Idiopathic Calcium Nephrolithiasis

1996 ◽  
Vol 91 (3) ◽  
pp. 313-318 ◽  
Author(s):  
Martino Marangella ◽  
Corrado Vitale ◽  
Michele Petrarulo ◽  
Lidia Rovera ◽  
Franca Dutto
Keyword(s):  
Drinking Water ◽  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Calcium Oxalate ◽  
Calcium Intake ◽  
Mineral Water ◽  
Stone Formation ◽  
Low Calcium ◽  
High Calcium ◽  
Markers Of Bone Resorption

1. To assess whether the mineral content of drinking water influences both risk of stone formation and bone metabolism in idiopathic calcium nephrolithiasis, 21 patients were switched from their usual home diets to a 10 mmol calcium, low-oxalate, protein-controlled diet, supplemented with 21 of three different types of mineral water. Drinking water added 1, 6 and 20 mmol of calcium and 0.5, 10 and 50 mmol of bicarbonate respectively to the controlled diet. 2. The three controlled study periods lasted 1 month each and were separated by a 20 day washout interval. Blood and urine chemistries, including intact parathyroid hormone, calcitriol and two markers of bone resorption, were performed at the end of each study period. The stone-forming risk was assessed by calculating urine saturation with calcium oxalate (βCaOx), calcium phosphate (βbsh) and uric acid (βUA). 3. The addition of any mineral water produced the expected increase in urine output and was associated with similar decreases in βCaOx and βUA, whereas βbsh varied marginally. These equal decreases in βCaOx, however, resulted from peculiar changes in calcium, oxalate and citrate excretion during each study period. The increase in overall calcium intake due to different drinking water induced modest increases in calcium excretion, whereas oxalate excretion tended to decrease. The changes in oxalate excretion during any one study period compared with another were significantly related to those in calcium intake. Citrate excretion was significantly higher with the high-calcium, alkaline water. 4. Parathyroid hormone, calcitriol and markers of bone resorption increased when patients were changed from the high-calcium, alkaline to the low-calcium drinking water. 5. We suggest that overall calcium intake may be tailored by supplying calcium in drinking water. Adverse effects on bone turnover with low-calcium diets can be prevented by giving high-calcium, alkaline drinking water, and the stone-forming risk can be decreased as effectively as with low-calcium drinking water.

scholarly journals Effect of a Low Calcium Dialysate on Parathyroid Hormone Secretion in Diabetic Patients on Maintenance Hemodialysis

2010 ◽  
Vol 15 (5) ◽  
pp. 927-935 ◽  
Author(s):  
Roberto Holgado ◽  
Henry Haire ◽  
Dennis Ross ◽  
Stuart Sprague ◽  
Madeleine Pahl ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Hormone Secretion ◽  
Maintenance Hemodialysis ◽  
Diabetic Patients ◽  
Low Calcium

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.

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