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PubMed1981

The arterio-venous difference for immunoreactive parathyroid hormone and the production of adenosine 3,'5'-monophosphate by isolated perfused bone: studies with analogs of parathyroid hormone.

Recent studies suggest that the uptake of immunoreactive parathyroid hormone (iPTH) displays different characteristics in liver, kidney, and bone. Using the isolated perfused canine bone, we have characterized the uptake of two synthetic analogs of PTH, bovine PTH-(3-34) [bPTH-3(3-34)] and [Nle8,Nle18,Tyr34]bPTH-(3-34) amide, which had previously been shown to inhibit PTH-stimulated adenylate cyclase activity in renal membranes. During the infusion of synthetic bPTH-(1-34) (3 ng/ml), extraction of iPTH by isolated perfused bone averaged 37 +/- 1%, and cAMP production rose from 6.2 +/- 2.0 to 21 +/- 3 pmol/min. Extraction of bPTH-(3-34) was similar (35 +/- 2%), but cAMP levels did not increase over baseline with PTH concentrations as high as 100 ng/ml. Simultaneous infusion of bPTH-(1-34) and bPTH-(3-34) at molar ratios of 1:2 led to a 50% inhibition of PTH-stimulated cAMP increases. The extraction by bone of the more potent in vitro inhibitor of renal cortical adenylate cyclase [Nle8,Nle18,Tyr34]bPTH-(3-34) NH2 (3 ng/ml) averaged 39 +/- 2%. In contrast, cAMP production rose from a baseline of 5.6 +/- 0.5 to 12.5 +/- 2.0 pmol/min, demonstrating agonist activity for the analog. These studies show that [Nle3,Nle18,Tyr34]bPTH-(3-34) NH2 has agonist properties in isolated perfused bone, and unsubstituted bPTh-(3-34) inhibits PTH-stimulated cAMP release by perfused bone.

Animals↗
PubMed1977

Secretion of parathyroid hormone by abnormal human parathyroid glands in vitro.

The secretory response of abnormal parathyroid glands obtained surgically from eleven patients with primary and secondary hyperparathyroidsm was tested in vitro. Short term flask studies were used to measure release of parathyroid hormone (PTH) at high (3.0 mM) and low (0.5 mM) calcium. Of eight adenomas, all but one showed increased release of hormone when exposed to low calcium ("responsive to calcium"), the degree of stimulation at three hours ranging from 15 to 209%. By comparison, two normal human glands were stimulated an average of 180%. Glands from three patients with secondary hyperplasia were also responsive to calcium. Thus, parathyroid glands from patients with primary and secondary hyperparathyroidism were characterized by a spectrum of responsiveness to calcium, and absolute "autonomy" was unusual. Even at high calcium concentrations, hormone release persisted at a low but definite level ("basal secretion"). The total number of functioning parathyroid cells is therefore a principal determinant in the oversecretion of PTH in hyperparathyroidism.

Adenoma↗
PubMed1988

[Immunoreactive parathyroid hormones in the circulation and cerebrospinal fluid from patients with renal failure: possible restriction of parathyroid hormone by the blood-brain barrier].

There are reports that patients with renal failure have elevated circulating concentrations of parathyroid hormone (PTH), which is suspected to be a causal factor of the cerebral symptoms of these patients. A positive correlation between the circulating level of immunoreactive PTH and the extent of abnormality in the electroencephalogram (EEG) in humans has been reported. Moreover, in uremic dogs normalization of the EEG was observed after parathyroidectomy, and increased abnormality of the EEG was observed on infusion of PTH. If PTH is really a causal factor of uremic encephalopathy and abnormality of the EEG in patients with renal failure, the question arises as to whether PTH acts on the brain after penetrating through the blood-brain barrier or in some other way. In this work, we measured PTH by both C-terminal-specific RIA (C-PTH) and N-terminal-specific RIA (N-PTH) in the circulation and cerebrospinal fluid (CSF) of normal subjects and patients with renal failure. Blood and CSF samples were obtained from 7 normal volunteers (31 approximately 81 years old: 4 males and 3 females) and 22 patients with chronic renal failure (25 approximately 87 years old: 12 males and 10 females). No patients had a psychotic disease or endocrinopathy other than secondary hyperparathyroidism. Samples of venous blood were collected from the subjects after an overnight fast at the time of lumbar puncture for CSF sampling. C-terminal-specific RIA for measurement of the plasma and CSF concentrations of C-PTH was carried out using a commercially available RIA kit (Eiken Laboratory Inc., Tokyo, Japan).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Dual effects of a new hypocalcemic agent, WR-2721, on cytoplasmic Ca2+ and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism.

The effects of the new hypocalcemic agent, WR-2721, on calcium-regulated parathyroid hormone (PTH) release, cytoplasmic Ca2+ (Ca2+i) and membrane potential were measured in dispersed parathyroid cells from patients with hyperparathyrodisim (HPT). The drug had no effects in the absence of extracellular Ca2+ but acted synergistically with Ca2+ in the 0.5-1.5 mM range by depolarizing the cells, increasing Ca2+i and inhibiting PTH release. Although the depolarizing effect of 3.0 mM Ca2+ was unaffected by WR-2721 the drug antagonized the effect of Ca2+ by decreasing Ca2+i and stimulating PTH release. Whereas the inhibitory actions of WR-2721 on PTH release may result from the activation of the mechanism for Ca2+ gating in the parathyroid cell plasma membrane, the stimulatory effect probably reflects increased intracellular Ca2+ sequestration. The drug is considered potentially important for the treatment of HPT.

Amifostine↗
PubMed1984

Prolactin stimulation of parathyroid hormone secretion in bovine parathyroid cells.

Previous studies have suggested that prolactin (PRL) may affect calcium (Ca) homeostasis by an action on vitamin D metabolism. In this study, the effects of PRL on parathyroid hormone (PTH) secretion were investigated in dispersed bovine parathyroid cells (PTC). PRL (0.013-1.3 microM) caused concentration-dependent increases in PTH secretion. PRL-stimulated PTH release was apparent as early as 1 h and was progressive thereafter for up to 3 h. PRL enhanced PTH release over a wide range of ambient Ca concentrations (0.5-2.0 microM). Ovine and rat PRL were more effective than bovine PRL in stimulating PTH secretion. This effect was apparently specific for PRL because neither ovine nor bovine growth hormone stimulated PTH secretion. PRL-stimulated PTH release was not mediated through the beta-adrenergic or dopaminergic receptor systems of PTC and was not associated with increased adenosine 3',5'-cyclic monophosphate (cAMP) levels. This study demonstrated a direct effect of PRL to stimulate PTH secretion in vitro. Although these data do not provide evidence for an effect of PRL in vivo, we suggest a mechanism by which PRL may influence parathyroid function and Ca homeostasis in the bovine species.

Adrenergic beta-Agonists↗
PubMed1982

Potassium stimulates parathyroid hormone release from perifused parathyroid cells.

A method for perifusing dispersed bovine parathyroid cells is described. Using this approach, we have studied the effects of raised extracellular potassium and ouabain on calcium-regulated parathyroid hormone (PTH) secretion in vitro. Decreasing calcium from 1.5 to 0.5 mM stimulated PTH release within 5-10 min, and the increased secretory rate was maintained for the duration of the low calcium administration. High potassium (60 mM) promptly stimulated PTH secretion at 1.5 mM calcium. The effect of high potassium was more transient than that of low calcium. Raised potassium significantly enhanced the response to 0.5 mM calcium. Ouabain (10(-3) M) had no significant effect at 1.5 mM calcium, but depressed the secretory response to 0.5 mM calcium. In conclusion, the effect of raised potassium on parathyroid cells is qualitatively similar to its effect on other endocrine and exocrine systems.

Animals↗
PubMed1986

Normalizing effect of Ca2+ ionophore on cytoplasmic Ca2+ and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism.

The effects of the Ca2+ ionophore A23187 on parathyroid hormone (PTH) secretion and cytoplasmic free Ca2+ concentration (Ca2+i) were measured at different extracellular Ca2+ concentrations using dispersed cells from patients with hyperparathyroidism (HPT). The addition of a low concentration of the Ca2+ ionophore to quin2-loaded cell preparations resulted in the apparent normalization of calcium-regulated Ca2+i. At all extracellular calcium concentrations Ca2+i reached significantly higher values in the presence of the ionophore and the dose-response relationship was shifted to the left. Under similar conditions calcium-regulated PTH release was correspondingly corrected with an increased suppressibility and left-shifted dose-response relationship. The data render strong support for a disturbed regulation of Ca2+i as a major factor in the pathophysiology of HPT.

Aminoquinolines↗
PubMed1986

Alteration in density, morphology and parathyroid hormone release of dispersed parathyroid cells from patients with hyperparathyroidism.

Dispersed parathyroid cells from normal human and bovine glands and from 10 patients with primary (7 adenomas, 3 hyperplasias) and 4 patients with uraemic hyperparathyroidism (HPT) have been investigated with respect to density, morphology and parathyroid hormone (PTH) release. Percoll density gradients enabled an efficient isolation of viable parathyroid cells which generally banded between 1.035-1.090 g/ml. The average density was significantly higher in cells from the normal than the abnormal glands. The pathological glands contained large chief cells, oxyphil and transitional oxyphil cells and, in one case, water-clear cells which were enriched in fractions with densities below 1.055 g/ml. Measurements of cell diameters revealed an increased proportion of enlarged cells in the preparation of abnormal glands. Nuclear diameters were similar in the normal human glands, adenomas and hyperplasias, but the variability was greater among the adenomas. In comparison to normal bovine parathyroid cells, PTH release of cells from the pathological human glands was reduced and abnormally insensitive to extracellular calcium. The oxyphil and water-clear cells secreted similar amounts of PTH as the chief cells of the abnormal glands. The disturbed PTH release in secondary HPT seemed to be confined mainly to cells within nodules of the hyperplastic glands. The results show that the disturbed hormone regulation in HPT is related to morphological changes of the cells and that buoyant density gradients can be used to accumulate the abnormal cells.

Adenoma↗
PubMed1987

Monoclonal antibody-mediated modulation of parathyroid hormone secretion by dispersed parathyroid cells.

Available data suggest that ionized calcium may interact with a cell surface "sensor" or "receptor" to produce changes in one or more intracellular second messengers that ultimately regulate the release of parathyroid hormone (PTH). Recently, we developed a series of monoclonal antibodies directed toward specialized differentiation antigens expressed on endocrine cells. Since many of these monoclonal antibodies displayed exquisite specificity for cell surface molecules on the parathyroid cell, we used these reagents as probes to investigate signal recognition/transduction mechanisms associated with abnormal calcium-regulated PTH secretion. Depending on their binding site on the respective target antigen molecules, these monoclonal antibodies either stimulated or inhibited hormone secretion. Thus, defects in membrane-associated structures may contribute to deranged calcium-regulated PTH secretion in abnormal parathyroid cells.

Antibodies, Monoclonal↗
PubMed1986

Parathyroid hormone (PTH) assay of parathyroid cysts examined by fine-needle aspiration biopsy.

The authors report three cases of parathyroid cysts examined by the fine-needle aspiration biopsy technic. A presumptive diagnosis of parathyroid cyst was made when characteristic water-clear fluid was aspirated. The diagnosis was then confirmed by parathyroid hormone (PTH) assay. The authors believe that the C-terminal/midmolecule determination should be the assay of choice, because the N-terminal-specific assay gave normal or slightly elevated results in all the cases studied. If only an N-terminal-specific PTH assay is obtained, potential for a false negative diagnosis exists. With a correct PTH assay, a specific diagnosis of parathyroid cyst can be rendered, which enables appropriate treatment of total fluid aspiration, which thereby eliminates the need for thyroid hormone treatment or surgery in most cases. A discussion of PTH assays is presented along with speculations concerning the secretion of PTH by the parathyroid gland. The previous literature detailing cytologic findings and the PTH assays of parathyroid cysts diagnosed by the fine-needle aspiration biopsy are reviewed.

Adult↗
PubMed1978

Role of anions in parathyroid hormone release from dispersed bovine parathyroid cells.

It is known that permeant anions are required for the release of epinephrine from isolated chromaffin granules and of serotonin from intact platelets. We have now investigated the role of anions in the release of a polypeptide hormone, parathyroid hormone, from dispersed bovine parathyroid cells. The release is inhibited 60%-80% by decreasing either [Cl-] or [OH-] and 60%-70% by replacement of NaCl with the impermeant anion isethionate. By contrast, substitution of various monovalent cations in the medium had no effect on the release. Disodium 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) and probenecid, which are known to block anion transport in the erythrocyte, also cause a dose-dependent 90%-100% inhibition of release. Moreover, kinetic analysis of inhibition by probenecid suggests that it is competitive with respect to either OH- or Cl-. These results suggest that anions and the anion transport system may play a role in exocytosis of a polypeptide hormone. The proton ionophore carbonyl cyanide p-trifluoromethoxyphenylhydrazone was was also found to block hormone release, and the possibility is discussed of a "chemosmotic" mechanism for exocytosis in this system similar to that previously postulated for chromaffin granules and platelets.

Animals↗
PubMed1984

Relation between parathyroid hormone and adrenocorticotropic hormone in primary hyperparathyroidism.

Parathyroid hormone is concerned with urolithiasis, and regulated by serum ionized calcium concentration. We thought that parathyroid hormone might also be regulated by a hormone. 1 mg of ACTH injection was given intramuscularly to 6 patients with primary hyperparathyroidism, 6 patients with urolithiasis, and 5 control subjects. Serum calcium significantly increased 2 h after ACTH injection in primary hyperparathyroidism. However in the other two groups, an increase of serum calcium was not observed. Parathyroid hormone increased after ACTH injection in most subjects of all three groups. Calcium concentration in a culture medium of parathyroidectomy increased in 4 cases, and the parathyroid hormone concentration in the culture medium increased in 3 cases after ACTH addition. From these data, we believe that ACTH directly influences the parathyroid glands, and that calcium is released from the parathyroid cells. Therefore, the decrease in calcium concentration in the parathyroid cells activates the excretion of parathyroid hormone. The fact that serum parathyroid hormone increases in most subjects in all groups supports our hypothesis, namely that ACTH acts directly on the parathyroid gland.

Adenoma↗
PubMed1977

Mechanism of resistance to the phosphaturic effect of the parathyroid hormone in the hamster.

The effect of parathyroid hormone and calcitonin on the renal excretion of phosphate, calcium, and cyclic AMP was evaluated in the thyroparathyroidectomized hamster, a mammal apparently reisstant to the phosphaturic effect of parathyroid hormone. Parathyroid hormone did not increase phosphate excretion, although it decreased excretion of calcium and increased urinary excretion of cyclic AMP. This lack of a phosphaturic response to parathyroid hormone was not reversed by administration of 25-OH vitamin D or infusions of calcium or phosphate. Calcitonin, another potentially phosphaturic hormone, also vailed to increase phosphate excretion but markedly elevated urinary excretion of cyclic AMP. In hamsters pretreated with infusion of urinary ammonium chloride, which decreased plasma and urinary pH, both parathyroid hormone and calcitonin increased excretion of phosphate as well as that of cyclic AMP. Acetazolamide had no phosphaturic effect in ammonium chloride-loaded hamsters, and it decreased cyclic AMP and calcium excretion. Alkalinization of urine by acetazolamide did not prevent the phosphaturic effect of parathyroid hormone in ammonium chloride-loaded hamsters, but it blocked the increase in urinary cyclic AMP excretion. Parathyroid hormone and calcitonin both stimulated adenylate cyclase in a cell-free system (600-g pellet) from hamster renal cortex, elevated tissue cyclic AMP levels, and activated protein kinase in tissue slices from hamster renal cortex. In acid medium, the increase in cyclic AMP and activation of protein kinase in response to parathyroid hormone was diminished, but addition of acetazolamide restored responsiveness of both parameters to control values. Acetazolamide, on the other hand, did not influence adenylate cyclase or its response to parathyroid hormone or cyclic AMP phosphodiesterase activity. We conclude that the lack of a phosphaturic effect of parathyroid hormone and calcitonin in the hamster depends on steps in the cellular action of these hormones, steps that are sensitive to pH subsequent to cyclic AMP generation and protein kinase activation. In addition, acetazolamide may potentiate the phosphaturic effect of parathyroid hormone by promoting accumulation of cyclic AMP in tissue. Thus, the hamster is a particularly useful model for studies of syndromes in which there is renal resistance to phosphaturic hormones.

3',5'-Cyclic-AMP Phosphodiesterases↗