scholarly journals Interactions between Calciotropic Hormones

1987 ◽  
Vol 80 (8) ◽  
pp. 478-480
Author(s):  
J N Bradbeer
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Dehydrogenase Activity ◽  
Steroid Hormone ◽  
Vitamin D Metabolites ◽  
Hormone Action ◽  
Calciotropic Hormones ◽  
Cytochemical Bioassay ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Dose Dependent

The metatarsal cytochemical bioassay (CBA) for parathyroid hormone (PTH) was adapted to study interactions between PTH and certain vitamin D metabolites. Thus, while they had no effect in the system alone, both 1,25(OH)2D3 and 25(OH)D3 caused a dose-dependent potentiation of PTH-stimulated glucose 6-phosphate dehydrogenase activity in the hypertrophic chondrocytes of the rat metatarsal. 1,25(OH)2D3 was about 1000 times more potent than 25(OH)D3. Specificity is indicated by the lack of a similar effect when either oestradiol or 1,24,25(OH)3D3 or a lactone derivative of 1,25(OH)2D3 was used. Furthermore, the rapidity of the effect of 1,25(OH)2D3 and 25(OH)D3, within 8 minutes, favours a membranophilic mechanism rather than the conventional nuclear mechanism of steroid hormone action.

Circulating levels of calciotropic hormones during treatment with nasal salmon calcitonin

1991 ◽  
Vol 125 (2) ◽  
pp. 127-131 ◽  
Author(s):  
Gorm Thamsborg ◽  
Tommy L. Storm ◽  
Henrik Daugaard ◽  
Søren Schifter ◽  
Ole H. Sørensen
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Nasal Spray ◽  
Salmon Calcitonin ◽  
Serum Levels ◽  
Treated Group ◽  
Human Calcitonin ◽  
Vitamin D Metabolites ◽  
Calciotropic Hormones ◽  
Circulating Levels

Abstract. Circulating levels of calciotropic hormones were measured during one year of treatment with either 200 IU of salmon calcitonin daily or placebo as a nasal spray in 20 postmenopausal women with a former Colles' fracture. A supplement of 0.5 gram elemental calcium was given to all participants. Serum levels of parathyroid hormone and human calcitonin were determined with radioimmunoassays, and serum levels of vitamin D metabolites were determined with protein binding assays. We did not find any significant differences between the two groups with respect to serum levels of calciotropic hormones. In the salmon calcitonin treated group there was a tendency towards a small decrease in serum levels of human calcitonin and an increase in serum levels of calcitriol. Our results suggest that treatment with 200 IU of salmon calcitonin daily as a nasal spray does not markedly affect fasting serum levels of parathyroid hormone, human calcitonin, and vitamin D metabolitis.

1,25(OH)2D3 blunts hormone-elevated cytosolic Ca2+ in osteoblast-like cells

1992 ◽  
Vol 263 (6) ◽  
pp. E1070-E1076
Author(s):  
J. Green ◽  
C. R. Kleeman ◽  
S. Schotland ◽  
L. H. Ye
Keyword(s):  
Vitamin D ◽  
Plasma Membrane ◽  
Bone Cell ◽  
Free Calcium ◽  
Osteoblastic Cell ◽  
Cell Physiology ◽  
Vitamin D Metabolites ◽  
Osteoblastic Cell Line ◽  
Calciotropic Hormones ◽  
Dihydroxyvitamin D

Cytosolic free calcium ([Ca2+]i) is an important regulator of bone cell physiology. We studied the interaction of vitamin D metabolites on the hormonal-activated Ca message system in the osteoblastic cell line UMR-106. The acute rise in [Ca2+]i induced by different calciotropic hormones [parathyroid hormone, prostaglandin E2 (PGE2)] was dose dependently blunted by 1,25-dihydroxyvitamin D [1,25(OH)2D3; half-maximal inhibitory concn approximately 5 x 10(-11) M] and was initially observed after 8 h of preincubation. The 1,25(OH)2D3 metabolite of vitamin D was two orders of magnitude more potent than 24,25(OH)2D3 and 25(OH)D3. To discern between an effect of 1,25(OH)2D3 on hormonal-induced Ca2+ entry through the plasma membrane channel vs. release of Ca2+ from internal stores, we suspended fura-2-loaded cells in Mn2+ rather than Ca2+ buffers. In cells preincubated with 1,25(OH)2D3, [Ca2+]i release (indicated by [Ca2+]i transient) was significantly blunted, whereas Mn2+ influx (indicating Ca2+ flux across the plasma membrane) was unaltered, suggesting a selective effect of 1,25(OH)2D3 on hormonal-activated release of Ca2+ from intracellular stores. 1,25(OH)2D3 also inhibited the PGE2-induced production of inositol 1,4,5-trisphosphate. We conclude that, in osteoblasts, chronic (hours) incubation with 1,25(OH)2D3 leads to attenuated stimulation of the [Ca2+]i transduction pathway by calciotropic hormones. This effect of 1,25(OH)2D3 may provide a cellular basis for the synergism between the effects of vitamin D and calciotropic hormones at the bone level.

Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro

1984 ◽  
Vol 105 (3) ◽  
pp. 354-359 ◽  
Author(s):  
Claes Rudberg ◽  
Göran Åkerström ◽  
Henry Johansson ◽  
Sverker Ljunghall ◽  
Jan Malmaeus ◽  
...  
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Parathyroid Tissue ◽  
Vitamin D Metabolites ◽  
Hormone Release ◽  
High Doses ◽  
Parathyroid Hormone Release ◽  
Dispersed Cells

Abstract. The effects of 125-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2–16 h. There was a gradual suppression of PTH release (5–55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.

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