Inhibition of Parathyroid Hormone Secretion by 25-Hydroxycholecalciferol and 24,25-Dihydroxycholecalciferol in the Dog

Canterbury, Janet M.; Lerman, Sidney; Claflin, Alice J.; Henry, Helen L.; Norman, Anthony W.; Reiss, Eric

doi:10.1172/jci109055

Cited by 142 publications

(46 citation statements)

References 36 publications

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“…these fragments in uremic animals is markedly proThe pronounced suppression of serum iPTH observed longed; the half-life is on the order of days in uremic in these studies confirms in intact animals what had animals as compared to hours in normal animals. In previously been demonstrated by perfusion of the thy-the study of Silverman and Yalow (19), the half-life roid-parathyroid apparatus of dogs (7)(8)(9). The impres-of COOH-terminal fragments appeared to be ofthe order sive feature of the suppression of iPTH in our experi-of weeks in an anephric man.…”

Section: Resultssupporting

confidence: 55%

“…Measurements were made in quadruplicates. Serum iPTH was assayed by methods previously described in great detail (7,(13)(14)(15). The antiserum used cross-reacted with intact hormone as well as NH2-and COOH-terminal fragments.…”

Section: Methodsmentioning

confidence: 99%

“…Our studies have been focused on the effects of vitamin D metabolites on PTH secretion in the dog (7,8) and this report represents an extension of previous investigations. Care et al (9) who pioneered the development of animal models for the study of PTH secretion, first reported evidence suggesting a suppressive effect of 24,25(OH)2D3 on PTH secretion.…”

Section: Introductionmentioning

confidence: 92%

“…In our model, the metabolite was infused directly into the thyroid artery and its volume of distribution was unknown. However, regardless of the assumptions that could be made about the volume of distribution, the doses used were clearly high (7).…”

Section: Introductionmentioning

confidence: 99%

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Metabolic Consequences of Oral Administration of 24,25-Dihydroxycholecalciferol to Uremic Dogs

Canterbury¹,

Gavellas²,

Bourgoignie³

et al. 1980

J. Clin. Invest.

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Section: Resultssupporting

confidence: 55%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Metabolic Consequences of Oral Administration of 24,25-Dihydroxycholecalciferol to Uremic Dogs

Canterbury¹,

Gavellas²,

Bourgoignie³

et al. 1980

J. Clin. Invest.

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“…Since the parathyroid glands possess specific receptors for 1,25(OH)2D3 (7) and a calcium binding protein (8), there is considerable interest in whether 1,25(OH)2D3 per se, independent of hypercalcemia, may play a role in the regulation of PTH secretion. To date, this issue remains controversial (9)(10)(11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.

Slatopolsky¹,

Weerts²,

Thielan³

et al. 1984

J. Clin. Invest.

678

292

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the serum calcium was increased by the oral administration of calcium carbonate, the decrement in serum i-PTH was only 25±6.65% when compared with 73.5±5.08% (P < 0.001) obtained by the administration of intravenous 1,25(OH)2D3. Thus, a similar serum calcium achieved by intravenous 1,25(OH)2D3 rather than calcium carbonate has a greater suppressive effect in the release of PTH.These studies indicate that 1,25(OH)2D3 administered intravenously rather than orally may result in a greater delivery of the vitamin D metabolite to peripheral target tissues other than the intestine and allow a greater expression of biological effects of 1,25(OH)2D3 in peripheral tissues. The use of intravenous 1,25(OH)2D3 thus provides a simple and extremely effective way to suppress secondary hyperparathyroidism in dialysis patients.

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Kidney and Bone: Physiological and Pathophysiological Relationships

Brown

1992

Comprehensive Physiology

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The sections in this article are: Chemical and Cellular Composition of Bone Extracellular Constituents of Bone Bone Cells Development and Structure of Bone Endochondral Ossification Intramembranous Ossification Skeletal Growth and Modeling Principles of Skeletal Growth Skeletal Modeling Epiphyseal Closure Bone Cell Function and Skeletal Growth and Modeling Bone Turnover and the Remodeling Cycle Skeletal Remodeling Cellular Control of Bone Remodeling Fracture Healing Bone Cell Function and Fracture Repair Interrelationships of Kidney and Bone in Normal Physiology General Considerations Overall Calcium Balance Hormonal Control of Mineral Ion Homeostasis Role of the Parathyroid Glands in the Calcium Homeostatic System Bone Cell Function and Ionic Homeostasis Aspects of Renal Function Essential for Normal Skeletal Structure and Function and Ionic Homeostasis Metabolic Bone Disease Osteitis Fibrosa Osteomalacia Osteoporosis Laboratory Evaluation of Metabolic Bone Disease Direct Assays of Calcium‐Regulating Hormones in Blood Clinical Assessment of the Function of Target Organs for Calcium‐Regulating Hormones Abnormalities in Renal Function Leading to Skeletal Disease Abnormalities in Renal Calcium Handling Abnormalities in Renal Phosphate Handling Hypo‐ and Hypermagnesemia Due to Renal Causes Renal Tubular Acidosis Primary Abnormalities in Vitamin D Metabolism Renal Resistance to PTH : Pseudohypoparathyroidism Chronic Renal Insufficiency Pathophysiology of Renal Osteodystrophy Disorders Affecting the Homeostatic Mechanisms Linking Kidney and Bone Primary Hyperparathyroidism Humoral Hypercalcemia of Malignancy Hypoparathyroidism Deficient Quantities and Action of Vitamin D Hypervitaminosis D Sarcoidosis and Other Granulomatous Diseases Other Hormonal Abnormalities and Drugs Affecting Both Bone and Kidney Calcitonin Growth Hormone Estrogen Glucocorticoids Insulin Thyroid Hormones Miscellaneous Associations Between Bone and Kidney Disorders Affecting Both Kidney and Bone Pharmacological Agents Affecting Both Kidney and Bone Effects of Bone Disease on the Kidney

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Inhibition of Parathyroid Hormone Secretion by 25-Hydroxycholecalciferol and 24,25-Dihydroxycholecalciferol in the Dog

Abstract: A B S T R A C T We studied the effects of vitamin

Cited by 142 publications

References 36 publications

Metabolic Consequences of Oral Administration of 24,25-Dihydroxycholecalciferol to Uremic Dogs

Metabolic Consequences of Oral Administration of 24,25-Dihydroxycholecalciferol to Uremic Dogs

Marked suppression of secondary hyperparathyroidism by intravenous administration of 1,25-dihydroxy-cholecalciferol in uremic patients.

Kidney and Bone: Physiological and Pathophysiological Relationships

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