Separation of the Hypocalcemic and Hypophosphatemic Actions of Calcitonin with Disodium Ethane-l-hydroxy-l,l-diphosphonate1

Talmage, Roy V.; Anderson, John J.B.; Kennedy, J. W.

doi:10.1210/endo-94-2-413

Cited by 21 publications

(4 citation statements)

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“…Thus bone cells exhibit a difference in handling of the mineral ions. Such differences have been noted by others using calcitonin to separate calcium and phosphate responses (Talmage, Anderson and Kennedy III 1974). Since these bones were cultured in a controlled Effect of PTH in the absence<A> and presence of acetazolamide Fig.…”

Section: Resultsmentioning

confidence: 80%

Acetazolamide Inhibition of Bone Resorption: Lack of Effect on Phosphate Release from Bone In Vitro

Wm¹,

Lc²

1981

Horm Metab Res

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Section: Resultsmentioning

confidence: 80%

Acetazolamide Inhibition of Bone Resorption: Lack of Effect on Phosphate Release from Bone In Vitro

Wm¹,

Lc²

1981

Horm Metab Res

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“…Indech and Jowsey [1971] and Mes ser and Copp [1974] have reported the per sistence of hypophosphataemia even after the loss of the hypocalcaemic response to calcitonin in kittens (receiving calcitonin up to 10 days) and rats (receiving calcitonin up to 42 days), respectively. According to Talmage et al [1974], the hypocalcaemic and hypophosphataemic effects of calcitonin are partially independent. The hypophosphataemic response includes extraosseus and extrarenal effects and involves an efflux of phosphate from plasma.…”

Section: Discussionmentioning

confidence: 99%

Effect of Calcitonin on Calcitonin Cells, Parathyroid Glands and Serum Electrolytes in the House Shrew (Suncus murinus)

Srivastav¹,

Swarup²

1982

Cells Tissues Organs

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Porcine calcitonin (CT) (0.5 MRC unit daily) was administered intraperitoneally to house shrews, Suncus murinus, for 42 days. The changes in serum calcium and phosphate levels as well as the light microscopical alterations of the parathyroid and calcitonin cells (C cells) between the 1st and 42nd day of treatment were recorded. The serum calcium level shows a fall up to the 7th day of treatment and thereafter it increases to normal values. The hypophosphataemic effect of CT increases progressively throughout the experiment continuing even after the loss of the hypocalcaemic effect. CT administration inhibits the release of secretory granules of C cells up to 21 days. Hyperplasia and degranulation of C cells is observed at 28, 35 and 42 days of treatment. C cells with collapsed membrane are also encountered in the lumina of the thyroid follicles. From the 28th day onwards the parathyroid chief cells of treated animals show hypertrophy and loss of staining reaction.

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“…Bone has been implicated as the site of action involved in the ability of EHDP to reduce the hypocalcemic effect of calcitonin [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15]. Since the loss of the hypocalcemic action of CT is accompanied by the loss of its ability to reduce the lead-induced hypercalcemia, bone appears to be the logical site of action of calcitonin on lead distribution.…”

Section: Discussionmentioning

confidence: 99%

A study of the action of calcitonin by its effects on lead-induced hypercalcemia

Talmage

VanderWiel

1979

Calcif Tissue Int

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Summary. Intravenous (i.v.) injection of lead acetate produces an immediate elevation in total plasma calcium and phosphate levels. This is due to the formation of calcium-phosphate compounds which can be removed by centrifugation at 25,000 • g. For this study, the effect of salmon calcitonin (CT) on these lead-induced plasma changes was studied. Intact male rats (175-250 g) were injected i.v. with lead acetate 10-30 mg/kg. Sodium acetateinjected rats served as controls. CT (0.1-0.2 mU/g) injected 30 min prior to lead modified the lead-induced plasma changes as follows: The concentration of lead remaining in plasma was statistically reduced. This was accompanied by a decrease in the amount of colloidal calcium-phosphate removed by ultracentrifugation and a corresponding decrease in the lead-induced elevation of total plasma calcium and phosphate levels. This action of CT was still effective in acutely nephrectomized rats. However, a 15-day pretreatment with a diphosphonate (20 mg EHDP/kg/day) abolished the hypocalcemic effect of CT and also abolished the ability of CT to affect the lead-induced plasma changes. Finally, CT was ineffective if injected in as short a time period as 30 min after lead injection.It is concluded from these studies that CT causes a rapid sequestering of lead from plasma into specific sites in bone. Previous reports show that within minutes after injection, CT causes the formation of calcium-phosphate complexes in fluid at the surfaces of bone and in osteocyte lacunae. It is postulated that lead reacts with these colloids (complexes) in a manner similar to its attachment to calcium and phosphate in plasma, thereby removing this lead from blood.Send qffprint requests to Dr. Roy V. Talmage at the above address.

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Separation of the Hypocalcemic and Hypophosphatemic Actions of Calcitonin with Disodium Ethane-l-hydroxy-l,l-diphosphonate¹

Cited by 21 publications

References 0 publications

Acetazolamide Inhibition of Bone Resorption: Lack of Effect on Phosphate Release from Bone In Vitro

Acetazolamide Inhibition of Bone Resorption: Lack of Effect on Phosphate Release from Bone In Vitro

Effect of Calcitonin on Calcitonin Cells, Parathyroid Glands and Serum Electrolytes in the House Shrew (<i>Suncus murinus</i>)

A study of the action of calcitonin by its effects on lead-induced hypercalcemia

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