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PubMed1982

Parathyroid hormone receptors in avian bone cells.

We have demonstrated binding of synthetic bovine parathyroid hormone (1-34) [bPTH-(1-34)] to embryonic avian bone cells in monolayer culture. The binding sites have qualitative and quantitative characteristics of a physiologically important parathyroid hormone (PTH) receptor. At apparent steady state (60 min at 24 degrees C), 5-10% of electrolytically labeled, receptor-purified 125I-labeled bPTH-(1-34) bound specifically to the cells whereas nonspecific binding was less than 1% of the added labeled hormone. Scatchard analysis showed a single order of PTH binding sites (Kd = 0.6 nM) with approximately 10,000 sites per cell. In this bone cell system, PTH bound to its binding site and stimulated cAMP accumulation over the same concentration range. Bovine PTH-(1-84) bound to the cells with the same apparent affinity as bPTH-(1-34).

Adenylyl Cyclases↗

PubMed1975

Skeletal resistance to endogenous parathyroid hormone in pateints with early renal failure. A possible cause for secondary hyperparathyroidism.

Studies were carried out to evaluate whether skeletal resistance to acute increments in endogenous parathyroid hormone exists in patients with mild to moderate renal insufficiency. Hypocalcemia was induced with the infusion of ethyl-enediamine-tetra-acetate (EDTA) in 10 normal subjects and 13 patients with mild renal failure. After the induction of hypocalcemia, the concentration of serum calcium increased gradually and reached preinfusion levels by 22 h in the normal subjects; in contrast, the levels of serum calcium in patients with mild renal insufficiency were significantly lower than the preinfusion values even at the end of 26 h following the EDTA infusion. This delayed recovery occurred despite significantly higher levels of serum immunoreactive parathyroid hormone (IPTH) in the patients than in the normal subjects. The increase in the levels of IPTH reflect elevations in the concentrations of biologically active hormone since urinary cyclic AMP increased significantly. Urinary calcium excretion following the EDTA infusion was not different in both groups and, therefore, could not account for the delayed recovery of serum calcium values in the patients with renal insufficiency. These results indicate that secondary hyperparathyroidism exists early in patients with renal failure and such patients have exaggerated parathyroid hormone secretion in response to acute hypocalcemia. The data are consistent with the concept that skeletal resistance to increments in endogenous parathyroid hormone is present in such patients. This abnormality is, at least partly, responsible for the hypocalcemia and secondary hyperparathyroidism of renal insufficiency.

Bone and Bones↗

PubMed1982

Role of parathyroid hormone and 1,25-dihydroxyvitamin D3 in the development of osteopenia in oophorectomized rats.

The effect of ovarian insufficiency on calcium metabolism has been thought to involve an increased bone resorptive effect of parathyroid hormone and possible impaired synthesis of 1,25-dihydroxyvitamin D3. In the present study a rat model allowing for controlled serum levels of parathyroid hormone and 1,25-dihydroxyvitamin D3 was used. Oophorectomy in this species is associated with increased serum levels of 1,25-dihydroxyvitamin D3 and decreased bone mass. Although thyroparathyroidectomy increased bone mass, an increased sensitivity of bone to parathyroid hormone in oophorectomized rats was not observed. Thus the development of the osteopenia did not seem to be related to increased parathyroid hormone sensitivity or to reduced levels of 1,25-dihydroxyvitamin D3. Exogenous 1,25-dihydroxyvitamin D3 increased bone mass in oophorectomized as well as intact rats. Intestinal calcium transport was increased by moderate doses of 1,25-dihydroxyvitamin D3. Intestinal calcium transport was also reduced by thyroparathyroidectomy and increased by the administration of parathyroid extract. A tendency for increased accumulation of 1,25-dihydroxyvitamin D3 in blood in oophorectomized rats has been noted. It is suggested that the tendency to hypercalcemia in ovarian-insufficient females given 1-hydroxylated vitamin D compounds may be related to a diminished metabolism of 1,25-dihydroxyvitamin D3.

Animals↗

PubMed1980

Parathyroid hormone release from the perfused canine thyroid-parathyroid complex isolated in situ.

A model for direct measurement of hormone release from the canine parathyroid gland is described. The two separate thyroid-parathyroid gland complexes were isolated in situ and perfused independently using a synthetic medium with a welldefined concentration of ionized calcium (Ca++). The concentration of parathyroid hormone (PTH) in the effluent was measured by radioimmunoassay, using an antiserum to bovine PTH that cross-reacts with canine PTH. Displacement curves of dilutions of effluent samples were similar to those of bovine PTH (1-84). During infusion of 1.49 mmol/l Ca++ the PTH release was constant for more than 4 h. Variations in Ca++ from 1.56 to 1.15 or 2.15 mmol/l induced rapid and sustained stimulation or suppression of PTH release. The retained ability of the preparation was ascertained by recording the response to infusion of calcium free medium at the end of each experiment.

Animals↗

PubMed1984

Cardiac actions and structural--activity relationship of parathyroid hormone on isolated frog atrium.

The hypercalcemic and hypotensive actions of parathyroid hormones (PTH), parathyroid extract, and synthetic PTH-(1-34) have been reported in many different animals. However, their cardiac action was only recognized recently. In the present study, experiments were designed to examine (1) whether PTH possesses any cardiac action on the isolated frog atrium, and (2) the importance of methionine and arginine of bPTH-(1-34) in cardiac action. Six different bPTH analogs were tested in frog atria in vitro: bPTH-(1-34); H2O2-treated bPTH-(1-34); [Nle8, Nle18, Tyr34]-bPTH-(1-34); H2O2-treated [Nle8, Nle18, Tyr34]-bPTH-(1-34); arginine-modified bPTH-(1-34); and arginine-regenerated bPTH-(1-34) (Nle-norleucine). bPTH-(1-34) produced positive chronotropic and inotropic responses. Oxidation with hydrogen peroxide abolished both actions of bPTH-(1-34). [Nle8, Nle18, Tyr34]-bPTH-(1-34) also possesses this cardiac-stimulating property. The H2O2 treatment of this analog did not alter the chronotropic action, but a decrease in the inotropic action was observed. The arginine-modified bPTH-(1-34) was much less potent than its native hormone, while the reversal of the arginine modification partially restored the biopotency. From these data, it is concluded that (1) bPTH-(1-34) possesses both positive chronotropic and inotropic effects on the frog atrium, (2) the cardiac actions of bPTH-(1-34) may be closely related with its hypotensive property, (3) methionines are not necessary for the cardiac actions, and (4) arginines are important for the cardiac-stimulating effects of bPTH.

Animals↗

PubMed1976

Somatostatin does not suppress plasma parathyroid hormone.

The effect of somatostatin on plasma parathyroid hormone (PTH) was studied in 6 subjects with normal parathyroid function and one patient with a parathyroid adenoma. In 5 subjects, including the one with the parathyroid adenoma, plasma PTH was measured by radioimmunoassay during a 4-hour infusion of somatostatin (500 mug/h). In 2 subjects, PTH responses to EDTA were compared with those observed during a simultaneous infusion of somatostatin and EDTA. In no instance was ther a discernible effect of the somatostatin infusion on plasma PTH. These results demonstrate that somatostatin does not suppress plasma PTH.

Adult↗

PubMed1981

Effect of furosemide on parathyroid hormone stimulated guinea pig renal adenylate cyclase and thyrotrophin and fluoride stimulated human thyroid adenylate cyclase.

The effect of furosemide 8 X 10(-4) mol/l an 8 X 10(-5) mol/l on parathyroid hormone stimulated adenylate cyclase was studied in renal tissue slices from guinea pigs. Furosemide caused a dose-dependent inhibition of the effect of parathyroid hormone on production of cyclic AMP, without having any significant effect on the basal cyclic AMP production. Furosemide in similar concentrations did not inhibit the stimulatory effect of thyrotrophin and fluoride in human thyroid homogenates suggesting that furosemide is not an universal inhibitor of adenylate cyclase and that the inhibition is not caused by a direct action of furosemide on the adenylate cyclase enzyme. Furosemide did not interfere with binding of cyclic AMP to cyclic AMP binding protein kinase from rabbit muscle. The results indicate that furosemide exerts an inhibitory influence either upon binding of parathyroid hormone to renal receptors or upon transmission of impulse from receptor to adenylate cyclase. The inhibitory influence of furosemide on parathyroid hormone action in kidney could explain the value of furosemide in the acute treatment of hypercalcaemia, but also suggest that chronic treatment with furosemide might interfere with normal calcium metabolism.

Adenylyl Cyclases↗

PubMed1997

Subacute infusion of physiological doses of parathyroid hormone raises blood pressure in humans.

BACKGROUND: Acute administration of parathyroid hormone (PTH) causes vasodilation and blood pressure decrease in experimental animals. This effect contrasts with the putative role of secondary hyperparathyroidism in the pathogenesis of hypertension of patients with renal failure. Uraemia is characterized by insulin resistance and hyperinsulinaemia. We therefore investigated whether subacute administration of physiological doses of human 1,34-PTH affects blood pressure under conditions of controlled insulin levels (euglycaemic clamp technique) in humans. METHODS: In a double-blind cross-over design 10 healthy male subjects received, on two occasions, in random order, for 2 h, either a sham infusion or an infusion of 200 units of 1,34-PTH. RESULTS: Mean ionized calcium concentration increased significantly (P < 0.01) within the normal range during euglycaemic hyperinsulinaemia, both with sham infusion (from 1.25 +/- 0.04 to 1.29 +/- 0.02 mmol/l) and with infusion of 1,34-PTH, but the increase was more marked with 1,34-PTH administration (from 1.26 +/- 0.05 to 1.33 +/- 0.07). In addition, mean platelet intracellular calcium concentration (by fluorescence spectroscopy) was unchanged with sham infusion (49.9 +/- 4.1 versus 50.3 +/- 5.0 nmol), but increased significantly (P < 0.05; paired t-test) after 1,34-PTH infusion (from 49.8 +/- 5.0 to 52.8 +/- 5.8). The infusion of 1,34-PTH resulted in a significant (P < 0.01) increase in mean MAP (from 84 +/- 5 to 88 +/- 5 mmHg) as compared with sham infusion (85 +/- 4 versus 86 +/- 4). The intra-individual changes in intracellular calcium concentration (delta[Ca2+]i) were significantly correlated to the changes in mean MAP (delta MAP) (r = 0.87, P < 0.001). In contrast to blood pressure, insulin sensitivity was not affected by 1,34-PTH infusion (M-value: 7.2 +/- 1.6 mg/kg per min) as compared with sham infusion (7.3 +/- 1.4). CONCLUSION: Subacute administration of physiological doses of parathyroid hormone under hyperinsulinaemic conditions significantly affects intracellular calcium and blood pressure in healthy subjects, but does not affect the action of insulin.

Adult↗

PubMed1971

Etiology of hyperparathyroidism and bone disease during chronic hemodialysis. II. Factors affecting serum immunoreactive parathyroid hormone.

Plasma concentration of immunoreactive parathyroid hormone (IPTH) was measured in 18 patients who had been on a hemodialysis program for longer than 6 months. A negative correlation was found between the predialysis plasma concentration of IPTH and the mean concentration of calcium in the dialysate previously used: plasma concentrations of IPTH were higher in patients dialyzed against a calcium concentration between 4.9 and 5.6 mg/100 ml than in patients dialyzed against a calcium concentration of 6.0 mg/100 ml or more. Plasma concentrations of IPTH also were higher in patients with bone disease than in patients without bone disease. Furthermore, a positive correlation was found between predialysis plasma concentrations of IPTH and calcium, and between mean predialysis concentration of IPTH and phosphate. To obviate the possibility that individual differences in susceptibility could have accounted for the observed effects of plasma phosphate and of dialysate calcium, a 2 x 2 factorial study was conducted in seven of these patients to examine the independent effects of perturbation of each of these factors. It was observed that plasma concentration of IPTH was lowest with the combination of high dialysate calcium and low plasma phosphate, highest with the combination of low dialysate calcium and high plasma phosphate, and intermediate with the two other combinations. It is concluded that both dialysate calcium and plasma phosphate are important determinants of parathyroid function in these patients.

Bone Diseases↗

PubMed1991

Vasoactive intestinal polypeptide stimulates parathyroid hormone release by interaction with cyclic adenosine monophosphate production of bovine parathyroid cells.

Influence of vasoactive intestinal polypeptide, neuropeptide Y, calcitonin gene-related peptide, and substance P was investigated on dispersed parathyroid cells of adult cattle. At a physiological concentration of extracellular calcium, vasoactive intestinal polypeptide stimulated the parathyroid hormone release in a dose-dependent manner, whereas no effects were noted for the other peptides. The dependency of PTH secretion upon extracellular calcium was shifted to the right by vasoactive intestinal polypeptide at 10(-6) mol/l, with a tendency for greater effects at low (0.5 mmol/l) than high concentrations (2.0-3.0 mmol/l) of the cation. Vasoactive intestinal polypeptide significantly enhanced cAMP release of the parathyroid cells, whereas no influence was noted on cytoplasmic calcium or pH within the cells. The results suggest that vasoactive intestinal polypeptide stimulates the PTH release by interaction with cAMP production of the parathyroid cells. This effect may contribute to the development of hypercalcemia in patients with neuroendocrine tumours secreting vasoactive intestinal polypeptide.

Animals↗

PubMed1989

The circadian rhythm of intact parathyroid hormone (1-84) and nephrogenous cyclic adenosine monophosphate in normal men.

A pronounced circadian rhythm has been demonstrated for intact parathyroid hormone (1-84) in the serum of normal male adults. The broad nocturnal rise of parathyroid hormone (1-84) secretion appears to be of physiological significance, for it is accompanied by a significant rise in nephrogenous cyclic adenosine monophosphate. The rate of return of parathyroid hormone (1-84) to baseline concentrations varies between individuals, an observation which has implications for the optimal time of sampling for the investigation of possible mild hyperparathyroidism.

Adult↗

PubMed1972

Calcemic fraction-A: biosynthetic peptide precursor of parathyroid hormone.

Calcemic fraction-A (CF-A) is a biologically active, hypercalcemic and bone resorptive peptide, which was detected in, and isolated from, bovine parathyroid glands [Hamilton et al. (1971) Endocrinology 89, 1440-1447]. It has been further purified, and its relationship to parathyroid hormone clarified. The peptide is present in fresh glands at a concentration of about 3 mug/g (parathyroid hormone, 100 mug/g). It contains 109 amino acids (hormone, 84), each of which is present in equal or greater molar ratio than in the hormone. Its molecular weight, calculated from amino-acid composition, is 12,144; determined by dodecyl sulfate-polyacrylamide gel electrophoresis, it is 12,500 (hormone, 9563). Per mole, it reacts with antiserum to parathyroid hormone to an extent of 7-10% that of the hormone, and is about 50% as active in its hypercalcemic and bone resorptive properties in the appropriate assays. Time course and pulse-chase experiments with parathyroid gland slices, in which the incorporation of amino acid into isolated peptide and hormone were measured, indicate that the hormone is made from a protein precursor; the patterns of incorporation of radioactivity are those that would be predicted from a precursor-product relationship. When the large peptide was incubated with parathyroid gland extracts it was partially converted to a molecule that appeared to be the hormone, as based upon its coelution with marker hormone from ion-exchange columns. Finally, tryptic digestion of the peptide increased the immunoreactivity of the sample in accord with the known greater immunoreactivity of the hormone than the peptide. On the basis of these results, it is proposed that the peptide is a biosynthetic precursor of the hormone in bovine parathyroid gland.

Acrylamides↗

PubMed1996

Clinical application of chemiluminescent immunoassay for thyroid stimulating hormone, free-T4 and intact-parathyroid hormone.

To meet the demands of clinical practice, rapid, sensitive and specific laboratory tests are essential. We evaluated the performance of a newer generation of chemiluminescent immunoassay (CLIA) system (Immulite, Diagnostic Products Corp, Los Angeles, CA, USA) and compared it with a popular immunoradiometric immunoassay (IRMA) system. The data of 158 patients whose thyroid function was assessed and that of another 158 patients whose parathyroid function was assessed were analyzed. The thyroid stimulating hormone (TSH) CLIA is an ultrasensitive TSH (us-TSH) assay that provides more detailed, reliable results for low TSH concentrations than TSH IRMA. Coupled with the free-T4 assay, the us-TSH assay enhances the ability to detect and monitor the status of thyroid dysfunction. Intact-parathyroid hormone (PTH) CLIA can detect lower serum intact-PTH levels, is more sensitive and is as reliable as IRMA. Combined with serum calcium levels and clinical conditions, it proved efficient and discriminated reliably between hypercalcemia associated with malignancy and that of hyperparathyroidism.

Humans↗

PubMed1978

[Hypercalcemia and biologically active parathyroid hormone].

Hypercalcaemia always results in serious clinical sequalae and, if not treated, carries a most unfavourable prognosis. The clinician will gain major diagnostic help from an evaluation of the calcitonin and parathyroid hormone blood levels. With regard to parathyroid hormone we have developed, for the first time, a radioimmunoassay which is specific for the estimation of biologically active hormone in the circulation. We are dealing here with an unusual radioimmunological situation as the immunochemical sites are generally quite distinct from those associated with hormonal activity. We are presenting in this first paper the normal values and also the variations that occur in different types of hypercalcaemia. The comparison of these results with those obtained by the usual methods of estimation for parathyroid hormone assay lacking in biological activity shows the value of this new technique.

Calcitonin↗

PubMed2004

Butyrate response factor 1 is regulated by parathyroid hormone and bone morphogenetic protein-2 in osteoblastic cells.

Parathyroid hormone (PTH) exerts potent and diverse effects in bone and cartilage through activation of type 1 PTH receptors (PTH1R) capable of coupling to protein kinase A (PKA) and PKC. We have used macroarrays to identify zinc finger protein butyrate response factor-1 (BRF1) as a novel PTH regulated gene in clonal and normal osteoblasts of human and rodent origin. We further demonstrate that in human osteoblast-like OHS cells, biologically active hPTH(1-84) and hPTH(1-34) stimulate BRF1 mRNA expression in a dose- and time-dependent manner, while the amino-terminally truncated hPTH(3-84) which does not activate PTH1R has no effect. Moreover, using specific stimulators or inhibitors of PKA and PKC activity, the PTH-elicited BRF1 mRNA expression is mediated through the PKA signaling pathway. In mouse calvarial osteoblasts, BRF1 mRNA levels are upregulated by PTH(1-84) and reduced in response to bone morphogenetic protein 2 (BMP-2). Hence, our data showing that BRF1 is expressed in osteoblastic cells and regulated by PTH and BMP-2, suggest an important role for BRF1 in osteoblasts within the molecular network of PTH-dependent bone remodeling.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1985

Immunocytochemical evidence for endogenous calcitonin and parathyroid hormone in osteoblasts from the calvaria of neonatal mice. Absence of endogenous estradiol and estradiol receptors.

Immunoreactivities to endogenous calcitonin, endogenous parathyroid hormone, endogenous estradiol and estradiol receptors were studied in osteoblasts from the calvaria of neonatal mice by immunocytochemistry with the use of ultrathin sections obtained by cryo-ultramicrotomy. Tissues were fixed in glutaraldehyde, postfixed in osmium tetroxide and frozen in liquid nitrogen. Estradiol and estradiol receptors could not be detected in osteoblasts, whereas calcitonin- and parathyroid hormone-like immunoreactivities were observed in this cell type. Calcitonin and parathyroid hormone had similar subcellular localizations: immunoreactivities were observed at the plasma-membrane level, in the cytoplasmic matrix, and in the nucleus. These results provide immunocytological evidence for: 1) the internalization of calcitonin and parathyroid hormone in osteoblasts; 2) a direct participation of calcitonin and parathyroid hormone in the regulation of osteoblasts; 3) the absence of estradiol receptors and estradiol in osteoblasts.

Animals↗

PubMed1977

Effect of ethane-1-hydroxy-1,1-diphosphonate (EHDP) on the ultrastructure of parathyroid glands and plasma immunoreactive parathyroid hormone in pregnant cows fed a low calcium diet.

The long term (70 days) effects of administering ethane-1-hydroxy-1,1-diphosphonate (EHDP) (4 mg. per kg. per day) on parathyroid function was investigated in pregnant cows fed a low calcium diet. Serum calcium and phosphorus were significantly lower at parturition and postpartum in EHDP-treated cows compared to pregnant control cows fed the low calcium diet. Plasma immunoreactive parathyroid hormone levels were similar prepartum, at parturition, and postpartum in cows administered EHDP and control cows. Immediately available calcium reserves were greater preparation in control cows than in cows receiving EHDP as indicated by a more rapid rate of return of serum calcium toward normal levels following ethylenediaminetetraacetic acid (EDTA)-induced hypocalcemia approximately 10 days prepartum. EHDP-treated cows responded to the hypocalcemic challenge with similar changes in plasma immunoreactive parathyroid hormone levels as in control cows; however, urinary hydroxyproline excretion increased at certain intervals only in control cows. Ultrastructurally, chief cells in parathyroid glands of both groups of cows were in an active stage of the secretory cycle with well developed organelles concerned with hormonela synthesis. Chief cells in cows administered EHDP were degranulated and contained fewer secretory granules in response to the hypocalcemia than those in control cows. Chief cells in EHDP-treated cows often had prominent perinuclear accumulations of microfilaments, scattered vacuolated mitochondria, and lysosomal bodies in the cytoplasm. Thyroid C-cells were densely granulated and thyroid calcitonin content was similar in both groups of cows. The principal defect in calcium homeostasis of EHDP-treated cows appeared to be an impairment both in bone calcium mobilization and bone matrix catabolism in response to the secretion of parathyroid hormone. In vitro uptake of 45Ca by duodenal mucosa and urinary excretion of cyclic adenosine monophosphate were similar in both groups of cows. The ability of the parathyroid glands to synthesize and secrete parathyroid hormone in response to hypocalcemia induced either by EDTA or associated with parturition was not impaired by the administration of EHDP.

Animals↗

PubMed1981

Acute effects of increased meat protein on urinary electrolytes and cyclic adenosine monophosphate and serum parathyroid hormone.

The effect of a high meat protein diet on urinary electrolytes, cyclic AMP, and serum immunoassayable parathyroid hormone was studied in six subjects fed a high meat protein diet (1.5 to 2.9 g/kg) for 7 days. The diet produced minor decreases in serum calcium and phosphorus but increased endogenous creatinine clearance by about 20% (p less than 0.02) and urinary calcium by about 80% (p less than 0.01) without changing urinary sodium. Urinary calcium correlated (p less than 0.01) with urinary sulfate (r = 0.60), ammonia (r = 0.72), and nitrogen (r = 0.60). Urinary cyclic AMP increased (p less than 0.01) 14% while serum parathyroid hormone (measured by C-terminal assays) decreased (p less than 0.05) by more than 30%. It was concluded 1) that this diet acutely altered renal handling of calcium at a site different from that of sodium, 2) that the excretion of acidic products of protein metabolism contributed to these changes, and 3) that parathyroid hormone secretion was not changed acutely.

Adult↗