Calcium and Phosphorus Homeostasis in the Parathyroidectomized Dog; Evaluation by Means of Ethylenediamine Tetraacetate and Calcium Tolerance Tests*

Sanderson, P. H.; Marshall, Foster; Wilson, Richard E.

doi:10.1172/jci104081

Cited by 67 publications

(23 citation statements)

References 10 publications

(7 reference statements)

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“…Nevertheless, the presence of a residual parathyroid activity cannot completely be excluded. It is well known that after transitory symptoms of parathyroid insufficiency, parathyroidectomized dogs recover after a few weeks a normal blood level of calcium (7) and cannot easily be distinguished from normal with regard to the renal excretion of phosphorus (8,9). The mechanism of the new homeostasis is not known.…”

Section: Resultsmentioning

confidence: 99%

Effect of Growth Hormone on Tubular Transport of Phosphate in Normal and Parathyroidectomized Dogs *

Corvilain¹,

Abramow²,

Bergans³

1964

J. Clin. Invest.

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It has been demonstrated recently that human growth hormone (HGH) increases the tubular reabsorption of phosphate in man (1, 2). This effect is probably responsible for the fall in urinary excretion of phosphate and the rise in plasma level of phosphorus produced by growth hormone (GH) and may also explain the elevation of plasma phosphorus found in acromegaly.The action of GH on tubular transport of phosphate is not necessarily a direct one. Since parathormone decreases maximal tubular reabsorption of phosphate (Tmpo4), GH might affect phosphate reabsorption by inhibiting the secretion of parathormone or by preventing its peripheral action.Indeed the first of these two hypotheses receives some support from metabolic studies: the enhancement of gastrointestinal absorption of calcium, which may occur during treatment with HGH (3), might be expected to inhibit parathyroid secretion.The present study has been undertaken to determine whether the action of GH on tubular transport of phosphate could be explained by a decrease in parathyroid secretion or in parathormone activity. For MethodsFemale dogs fed constant diets were used for these experiments. Renal studies were performed 22 hours after the last feeding. The dogs were unanesthetized. The bladder was catheterized with a rubber catheter that remained in place throughout the experiment. Five hundred ml of water was given by stomach tube to increase urine volume. Blood was drawn from an indwelling arterial needle for control blood phosphorus and creatinine.A priming dose of creatinine and phosphate was administered intravenously (20 ml of a 10% creatinine solution, 20 ml of a solution containing Na2HPO4 12 H20, 10%, and KH2PO4, 0.75%o). A sustaining solution containing creatinine and phosphate was then infused at a rate such that a gradual increase of the plasma phosphorus value in the range of 9 to 14 mg per 100 ml was obtained, and serum creatinine value of about 50 to 70 mg per 100 ml was reached.Thirty minutes after the infusion was begun, urine was collected for consecutive periods varying in length from 10 to 15 minutes. Blood was drawn from the artery at the mid-point of each period. Each collection was ended by washing the bladder twice with distilled water and air.After five collection periods, 300 U of PTH 1 was injected intravenously.The infusion of creatinine and phosphorus was maintained, and eight further collections of urine were performed. Three days after such an experiment, intramuscular injections of bovine GH2 were given once a day (1.5 mg per kg per day) for 8 days; on day 8 of treatment, the renal study was repeated. The

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Section: Resultsmentioning

confidence: 99%

Effect of Growth Hormone on Tubular Transport of Phosphate in Normal and Parathyroidectomized Dogs *

Corvilain¹,

Abramow²,

Bergans³

1964

J. Clin. Invest.

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“…It has been suggested that the drain upon the plasma calcium imposed by such sequestration results in low levels in the blood. However, this explanation alone fails to indicate why the plasma calcium is not replenished from skeletal reserves, as happens after experimentally induced hypocalcaemia (Sanderson et al, 1960;Potts et al, 1971).…”

Section: Discussionmentioning

confidence: 98%

The nature of hypocalcaemia in acute pancreatitis

McMahon

Woodhead

Hayward

1978

British Journal of Surgery

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A retrospective and prospective study was made of 82 attacks of acute pancreatitis occurring in 80 patients. Attacks were defined as mild (55) or severe (27) according to clinical criteria. Severe attacks were associated with significantly low levels of uncorrected calcium and calculated ionized calcium, both at the time of admission and 48 h later. Patients with severe attacks were found to have lower levels of parathyroid hormone than either those with mild attacks or other patients who had undergone an abdominal operation. These results indicate that severe pancreatitis is associated with true hypocalcaemia, and that deficiency of circulating parathyroid hormone may be a factor in its production.

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“…The hypocalcemia which resulted could readily be attributed to removal of the parathyroid glands; however, the impaired recovery of these animals from the effects of calcium infusions could not be readily explained by the prevailing concept of calcium regulation. Sanderson et ~~· (1960) did not realize the import of these findings. It remained for Copp and coworkers to evaluate the effects on systemic blood calQium of acute stimulation or suppression of parathyroid glandular activity.…”

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confidence: 90%

Calcitonin Activity of Particulate Fractions of the Ovine Thyroid Gland

Oeltgen¹,

L'Heureux²

1975

Horm Metab Res

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Mitochondria, nu dei, and microsomes obtained from ovine thyroid slices wh ich had been incubated in Krebs-Ringer bicarbonate buffer containing 4.8, 11.5 or 26.0 mg% concentration of calcium were assayed for calcitonin activity in rats. The microsomal preparatioa was the only particulate fraction to exhibit marked hypocalcemic activity and the hormonal activity of this fraction was enhanced by a 26.0 mg% calcium concentration in the incubation medium. The identity of the hypocalcemic species in the microsomal fraction with a calcitonin preparation 01' known potency was established by polyacrylamide gel eletrophoresis and by isoelectric focusing. The ovine microsomal calcitonin was resolved into two pro tein bands with isoelectric points (pl's) of 3.49 and 3.84. Both of these protein peaks exhibited hypocalcemic activity. The porcine standard calcitonin was resolved into two protein bands with pl's of 3.70 and 3.94.

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Calcium and Phosphorus Homeostasis in the Parathyroidectomized Dog; Evaluation by Means of Ethylenediamine Tetraacetate and Calcium Tolerance Tests*

Cited by 67 publications

References 10 publications

Effect of Growth Hormone on Tubular Transport of Phosphate in Normal and Parathyroidectomized Dogs *

Effect of Growth Hormone on Tubular Transport of Phosphate in Normal and Parathyroidectomized Dogs *

The nature of hypocalcaemia in acute pancreatitis

Calcitonin Activity of Particulate Fractions of the Ovine Thyroid Gland

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