Effect of parathyroid hormone on45Ca2+ accumulation neurosecretory cells and on blood vasopressin levels after parathyroidectomy and injection of parathyroid extract

1992 ◽  
Vol 113 (3) ◽  
pp. 289-291
Author(s):  
D. N. Khudaverdyan ◽  
A. A. Asratyan
Keyword(s):  
Parathyroid Hormone ◽  
Neurosecretory Cells ◽  
Parathyroid Extract

EFFECT OF GLUCAGON ON BONE COLLAGEN METABOLISM IN THE RAT

1972 ◽  
Vol 55 (2) ◽  
pp. 245-252 ◽  
Author(s):  
D. N. KALU ◽  
CARMEL HILLYARD ◽  
G. V. FOSTER
Keyword(s):  
Parathyroid Hormone ◽  
Renal Excretion ◽  
Physiological Role ◽  
Bone Collagen ◽  
Urinary Hydroxyproline ◽  
Parathyroid Extract ◽  
Relationship Of ◽  
The Relationship ◽  
Hydroxyproline Excretion

SUMMARY The effect of glucagon on bone was studied in rats. Urinary hydroxyproline excretion and incorporation of [3H]proline into bone hydroxyproline were used as indices of bone collagen breakdown and formation respectively. Parathyroid extract (15 USP units/rat/h, i.v.), infused into thyroparathyroidectomized animals, increased urinary hydroxyproline excretion. This increase was nullified by simultaneous administration of glucagon (50 μg/rat/h, i.v.). Rats treated with glucagon for 12 days (30 μg/100 g/day, s.c.) excreted slightly less hydroxyproline in their urine than controls. In both intact and thyroparathyroidectomized rats, glucagon (10 μg/100 g/h, s.c.) decreased incorporation of [3H]proline into bone. Similar results were obtained in nephrectomized rats, evidence that changes produced by glucagon were not solely due to alterations in proline pool size caused by increased renal excretion. From these data it is concluded that: (1) glucagon can inhibit bone resorption (the effect being slight in normal rats, but easily demonstrable in parathyroid hormone-treated thyroparathyroidectomized rats), (2) release of endogenous calcitonin is not required to produce this effect, (3) parathyroid hormone and glucagon may act on the same target cell in bone, (4) inhibition of skeletal resorption may contribute to glucagon-induced hypocalcaemia, and (5) the hormone possibly decreases bone formation. Since pharmacological doses of glucagon were used in our studies, the relationship of the observations made to the physiological role of glucagon is unknown.

ACQUIRED RESISTANCE TO PARATHYROID HORMONE

1976 ◽  
Vol 83 (2) ◽  
pp. 321-328 ◽  
Author(s):  
Tushar K. Sinha ◽  
Sherry F. Queener ◽  
Norman H. Bell ◽  
Sarah Larson
Keyword(s):  
Parathyroid Hormone ◽  
Renal Cortex ◽  
Acquired Resistance ◽  
Terminal Portion ◽  
Short Term ◽  
Clinical Resistance ◽  
Term Administration ◽  
Parathyroid Extract ◽  
Bovine Parathyroid Hormone

ABSTRACT Studies are presented in a patient with pseudohypoparathyroidism who showed a partial response to parathyroid extract. Resistance to the extract was observed after its short-term administration for the fourth time. Serum from the patient contained antibodies of the γG globulin class which bound 125I-labelled bovine parathyroid hormone. Prior incubation of parathyroid hormone with the serum prevented the activation in vitro of adenylate cyclase from pork renal cortex. The antibodies were directed primarily toward the C-terminal portion of the molecule. Thus, clinical resistance to parathyroid hormone is attributed to specific antibodies.

The Role of Parathyroid Hormone in the Gastro-Intestinal Absorption of Calcium

1970 ◽  
Vol 39 (1) ◽  
pp. 89-94 ◽  
Author(s):  
M. R. Wills ◽  
J. Wortsman ◽  
C. Y. C. Pak ◽  
F. C. Bartter
Keyword(s):  
Parathyroid Hormone ◽  
Intestinal Absorption ◽  
Calcium Absorption ◽  
Control Period ◽  
Normal Subjects ◽  
Parathyroid Extract

1. Gastrointestinal calcium absorption was studied in six normal subjects and in one patient with idiopathic hypoparathyroidism during a control period and during treatment with parathyroid extract. 2. In all subjects there was a small increase in the gastro-intestinal absorption of calcium during the administration of parathyroid extract.

DIFFERENTIAL STIMULATION BY PARATHYROID HORMONE OF BONE AND KIDNEY RIBONUCLEIC ACID SYNTHESIS

1971 ◽  
Vol 49 (3) ◽  
pp. 493-506 ◽  
Author(s):  
J. STEINBERG ◽  
G. NICHOLS
Keyword(s):  
Parathyroid Hormone ◽  
Specific Activity ◽  
Acid Synthesis ◽  
Hormonal Stimulation ◽  
Precursor Pool ◽  
Hormonal Effect ◽  
Parathyroid Extract ◽  
Apparent Shift ◽  
Stimulation Of

SUMMARY The effects of parathyroid extract (PTE) on the synthesis in vivo of free nucleotide and RNA were compared in rat metaphysial bone and kidney. The incorporation of 32P into chromatographically pure acid-soluble 5′-AMP and purified bulk RNA was examined at various times after PTE administration. Pulse-labelled RNA was further characterized by sedimentation in sucrose density gradients and by ribomononucleotide analysis. In both organs the labelling of 5′-AMP and its turnover were accelerated after administration of the hormone. The pool size of free AMP of kidney was approximately 3 times that of bone; neither was affected by PTE. The specific activity of pulse-labelled kidney AMP was always greater, and hormonal stimulation of its labelling was more rapid than in bone. Despite more extensive precursor labelling, the stimulation of renal RNA synthesis was negligible, and was delayed for several hours, the overall hormonal effect being inseparable from its effect on phosphate entry into the nucleotide precursor pool. In bone, the hormonal stimulation of RNA labelling was immediate, and continued to increase at a linear rate for up to 12 h. Initially, stimulation of RNA polymerization accounted for the total hormonal effect, while after 4 h an increasing proportion of the total increase in RNA labelling was attributable to enhanced precursor labelling. Newly synthesized bone RNA differed qualitatively from kidney RNA in its sedimentation properties and composition. Although the labelling of all RNA species and RNA-nucleotides in bone was stimulated by PTE, there was a proportionately greater effect on the labelling of ribosomal RNA, and an apparent shift towards GMP-rich molecules, neither change being manifest in kidney. It is concluded that while bone and kidney share certain mechanisms, they show changes in RNA biosynthesis in response to parathyroid hormone which are both quantitatively and qualitatively different and which are in accord with the RNA requirements for the respective physiological response of each.

Evidence for a direct effect of parathyroid hormone on urinary acidification

1965 ◽  
Vol 209 (3) ◽  
pp. 643-650 ◽  
Author(s):  
Dorothea E. Hellman ◽  
William Y. W. Au ◽  
Frederic C. Bartter
Keyword(s):  
Parathyroid Hormone ◽  
The Body ◽  
Hydrogen Ion ◽  
Renal Tubules ◽  
Titratable Acid ◽  
Urinary Acidification ◽  
Parathyroid Extract ◽  
Normal Women ◽  
Solute Excretion ◽  
Sodium And Potassium

The effects of intravenously administered parathyroid extract and of a purified parathyroid hormone on urinary acidification and on solute excretion were measured in six thyroparathyroidectomized dogs, in three normal women, and in a patient with diabetes insipidus. Parathyroid extract and the purified parathyroid hormone produced an immediate rise in urinary pH and bicarbonate with a fall in titratable-acid-minus-bicarbonate and in ammonia in all subjects. This was usually associated with a rise in urinary sodium and potassium. The changes in urinary acidification usually preceded any rise in glomerular filtration rate, and were associated with no increase in serum bicarbonate concentration. They also preceded a rise in the excretion of phosphate in most experiments, and thus did not depend on a rise in urinary buffer content. It is postulated that parathyroid hormone inhibits sodium-for-hydrogen ion exchange in the renal tubules, perhaps by interfering directly with the ability of the kidney to maintain a hydrogen ion gradient between the body fluids and the tubular urine.

Effects of parathyroid extract on metabolism of sulfate in immature rats

1960 ◽  
Vol 198 (3) ◽  
pp. 605-608 ◽  
Author(s):  
Felix Bronner
Keyword(s):  
Parathyroid Hormone ◽  
Bone Formation ◽  
Metabolic Activity ◽  
Calcium Mobilization ◽  
Long Bones ◽  
Chemical Analyses ◽  
Control Solution ◽  
Immature Rats ◽  
Parathyroid Extract

Administration of parathyroid extract to immature rats that had been given S35 24 hours earlier resulted on the average in a 30% increase in the level of S35 in the plasma, a 25% higher output of S35 in the urine, a 17% increase in the pelt content of S35, and a 14% increase in the ratio (S35 in humerus ends:S35 in humerus shafts), as compared with litter mates treated with an inactive control solution. The findings are interpreted as indicating that calcium mobilization induced by the action of parathyroid hormone proceeds by removal of both organic and inorganic portions of bone. Concomitant histological observations confirmed the inference drawn from the chemical analyses, namely, that administration of parathyroid extract induced a higher than normal metabolic activity in the ends of the long bones and resulted in increased bone formation and resorption.

Alterations in renal tubular phosphate transport during intravenous infusion of parathyroid extract in the dog

1959 ◽  
Vol 196 (3) ◽  
pp. 567-571 ◽  
Author(s):  
James G. Foulks ◽  
Florence A. Perry
Keyword(s):  
Parathyroid Hormone ◽  
Intravenous Infusion ◽  
Phosphate Transport ◽  
High Threshold ◽  
Phosphate Excretion ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Parathyroid Extract ◽  
Renal Tubular ◽  
Adequate Rate

The intravenous infusion of parathyriod extract at an adequate rate (1–4 u/kg/hr.) invariably leads to phosphaturia which is primarily the result of altered renal tubular transport of the ion. In the intact fasted dog, several hours may be required for the infusion of parathyroid extract to reduce the initially high threshold for endogenous phosphate excretion below the filtered phosphate load. Other procedures which reduce the threshold for phosphate excretion may accelerate the onset of phosphaturia under these circumstances. However, the sluggish nature of this response suggests that parathyroid hormone does not contribute to the rapid adjustments in renal tubular phosphate transport which accelerate phosphate excretion following phosphate administration.

Inhibition by calcitonin of bone resorption induced in vitro by vitamin A

1968 ◽  
Vol 170 (1018) ◽  
pp. 61-69 ◽  
Keyword(s):  
Parathyroid Hormone ◽  
Bone Resorption ◽  
Vitamin A ◽  
Kinetic Studies ◽  
Good Evidence ◽  
Plasma Calcium ◽  
Parathyroid Extract ◽  
Rat Thyroid

There is now good evidence for a thyroid polypeptide hormone, calcitonin, that lowers plasma calcium (Gudmundsson, MacIntyre & Soliman 1966). Bone was soon suspected as a primary site of action of this hormone, and Milhaud, Perault & Moukhtar (1965) concluded from kinetic studies with 45 Ca in rats that calcitonin lowers plasma calcium by inhibiting the resorption of bone. This theory of its action has received considerable support from investigations made both in vivo and in vitro . I propose to summarize the latter. In vitro studies by Friedman & Raisz (1965) showed that extracts of rat thyroid inhibit the release of calcium from embryonic long bones of rats; the effect was greatest when resorption was stimulated by parathyroid hormone. Aliapoulios, Goldhaber & Munson (1966) demonstrated that partially purified hog calcitonin can prevent the effects of parathyroid extract on mouse calvariae in vitro ; they also stated, without details, that calcitonin counteracted resorption of bone induced by vitamin A, thereby supporting the evidence from studies in vivo that the action of calcitonin is independent of that of parathyroid hormone. The results described by Gaillard (1966) can also be interpreted as supporting the theory that calcitonin acts by inhibiting bone resorption.

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