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PubMed2001

Inverse relation between mRNA synthesis and secretion of parathyroid hormone in athymic mice grafted with human parathyroid tissue.

Parathyroid hormone (PTH) mRNA in original and transplanted human adenomatous parathyroid tissue and human serum intact PTH (S-iPTH) was measured in athymic mice at 4, 7, 14, and 28 days after transplantation. Parathyroid tissue was obtained during surgery for hyperparathyroidism and implanted subcutaneously. PTH mRNA detection was done with RT-PCR followed by membrane blot and hybridisation and S-iPTH was analysed using a human specific immunoradiometric method. At 4 days, PTH mRNA was 79.6+/-5.3% (mean+/-SE) of that in original tissue whereas S-iPTH was only 5.4 ng/l. At 28 days, PTH mRNA was significantly reduced to 60.7+/-4.1% whereas S-iPTH was increased to 192 ng/l. The reduced PTH mRNA expression in the transplants at 28 days may be explained by an inhibited DNA transcription. The presence of human S-iPTH in transplanted mice at 4 days may be due to cell disintegration and diffusion. The gradual increase in S-iPTH during the experimental period probably reflects increased transplant cell volume and improved graft revascularisation.

Animals↗
PubMed1986

Calcium-dependent release of carboxyl-terminal fragments of parathyroid hormone by hyperplastic human parathyroid tissue in vitro.

The role of intracellular calcium in the secretion of fragments of PTH by human parathyroid tissue has not been examined previously. We used an in vitro perifusion system to study this phenomenon. Hyperplastic human parathyroid tissue, obtained at surgery from patients with chronic renal failure, was sliced into small pieces, placed in perifusion chambers, and exposed to low (0.5 mM) or high (2.0 mM) calcium concentrations. PTH secreted into the perifusion medium was analyzed by gel exclusion chromatography and RIA using a carboxyl-terminal antiserum. Under high calcium conditions, proportionally more carboxyl-terminal fragments of PTH (65.3%) were released by the perifused tissue than intact PTH (34.7%). When perifused with low calcium medium, the tissue released more intact PTH (55.0%) than carboxyl-terminal fragments (45.0%). These studies are consistent with the suggestion that calcium-dependent intracellular degradation of PTH plays an important role in the regulation of hormone secretion.

Adult↗
PubMed1988

Effects of calcium on synthesis and secretion of parathyroid hormone and secretory protein I.

Bovine parathyroid organoids were cultured for up to 3 wk in medium containing 1.4 or 1.8 mM calcium. Steady-state secretion of parathyroid hormone and secretory protein I was two- to fourfold greater at 1.4 mM. At the end of culture, organoids were incubated 3.5 h in 1 or 2 mM calcium to examine maximum and minimum acute secretory rates. Relative to organoids cultured at 1.8 mM calcium, culture at 1.4 mM induced a hypersecretory state, i.e., both the maximum and minimum acute secretory rates of organoids previously cultured at 1.4 mM calcium were up to threefold greater than those of organoids previously at 1.8 mM calcium. Proparathyroid hormone synthesis was up to 50% greater in organoids cultured at 1.4 mM calcium, whereas secretory protein I and total protein synthesis were unaltered. The results showed that parathyroid hypersecretion can be induced by chronic hypocalcemic conditions in vitro. We conclude that the secretory adaptation to chronic hypocalcemia in vitro involves alterations in both synthesis and degradation of parathyroid hormone.

Animals↗
PubMed1978

Effect of parathyroid hormone on plasma prolactin in man.

The iv infusion of parathyroid extract or the synthetic fragments of 1-34 bovine or human parathyroid hormone produced a rapid and marked increase of plasma PRL in normal subjects. The stimulation of the release of endogenous parathyroid hormone by administration of disodium EDTA also resulted in a parallel increase of plasma PRL. Parathyroid hormone did not act via plasma cAMP, as the plasma level reached by this nucleotide was too small to produce PRL release. The ingestion of L-dopa 2 h before parathyroid hormone infusion suppressed the PRL response, suggesting that dopamine and parathyroid hormone interact at a common site. As it has been recently shown that PRL stimulates the renal synthesis of 1,25-dihydroxycholecalciferol, the present data suggest that the effect of parathyroid hormone on this synthesis may be due to the increase in plasma PRL.

Adult↗
PubMed2006

Multihormonal resistance to parathyroid hormone, thyroid stimulating hormone, and other hormonal and neurosensory stimuli in patients with pseudohypoparathyroidism.

In patients with pseudohypoparathyroidism, hormonal resistance first affects parathyroid hormone (PTH), which leads to calcipenia, a decrease in renal vitamin D activation, and a tendency to bone receptor remodeling. However, because G proteins are ubiquitously distributed, multiple hormonal resistance occurs in pseudohypoparathyroidism type Ia and type Ic, impairing responses to other calciotropic hormones (PTHrP, calcitonin), TSH, and also pituitary and hypothalamic hormones, and to neurosensory stimuli. The diversity of multihormonal resistance contributes to the various phenotypes of the disease. Some clinical discomfort and medical consequences of the disease can be treated or prevented with hormone supplementation or modulation.

Hearing↗
PubMed2005

Intraoperative intact parathyroid hormone level monitoring as a guide to parathyroid reimplantation after thyroidectomy.

OBJECTIVE: The goal of this study was to determine whether intraoperative intact parathyroid hormone (IOiPTH) levels can predict the functional status of remaining parathyroids at the end of total thyroidectomy and thereby be a guide for parathyroid autotransplantation when glands are deemed not functional. STUDY DESIGN: Prospective study involving 23 patients undergoing either total thyroidectomy or completion thyroidectomy METHODS: During surgery, an attempt was made to identify all four parathyroid glands. Normal size vascular glands were preserved, whereas avascular glands were microdissected and reimplanted. Serial IOiPTH was measured preoperatively after each parathyroid was identified, manipulated, or removed and serum iPTH measurements were done postoperatively up to 56 days. RESULTS: The sensitivity of low IOiPTH in identifying a devascularized gland was 88.9%, and specificity was 92.9%. A normal IOiPTH level indicates at least two functioning glands. IOiPTH levels between 1.5 and 10 pg/mL indicate only one functional gland. Undetectable IOiPTH levels indicate no residual functioning gland. CONCLUSIONS: For patients undergoing total or completion thyroidectomy, IOiPTH should be routinely measured at the end of the procedure, and a level less than 10 pg/mL requires reassessment of remaining parathyroid glands. Vascularized glands should be preserved regardless of IOiPTH levels. Devascularized glands or glands of questionable vascularity should be considered for autotransplantation.

Humans↗
PubMed1983

Effects of parathyroid hormone on skeletal muscle protein and amino acid metabolism in the rat.

Because prominent skeletal muscle dysfunction and muscle wasting are seen in both chronic uremia and in primary hyperparathyroidism, and because markedly elevated parathyroid hormone levels occur in both disorders, potential effects of parathyroid hormone on skeletal muscle protein, amino acid, and cyclic nucleotide metabolism were studied in vitro using isolated intact rat epitrochlearis skeletal muscle preparations. Intact bovine parathyroid hormone and the synthetic 1-34 fragment of this hormone stimulated the release of alanine and glutamine from muscle of control but not from chronically uremic animals. This stimulation was dependent upon the concentration of parathyroid hormone added: At 10(5) ng/ml parathyroid hormone increased alanine release 84% and glutamine release 75%. Intracellular levels of alanine and glutamine were not altered by parathyroid hormone. Increasing concentrations of the 1-34 polypeptide decreased [(3)H]leucine incorporation into protein of muscles from both control and uremic animals. Using muscles from animals given a pulse-chase label of [guanido-(14)C]arginine in vivo, parathyroid hormone increased the rate of loss of (14)C label from acid-precipitable protein during incubation and correspondingly increased the rate of appearance of this label in the incubation media. Parathyroid hormone increased muscle cAMP levels by 140% and cGMP levels by 185%, but had no effect on skeletal muscle cyclic nucleotide phosphodiesterase activities as assayed in vitro. Adenylyl cyclase activity in membrane preparations from control but not uremic rats was stimulated by parathyroid hormone in a concentration-dependent fashion. However, no stimulation of guanylyl cyclase activity was noted by parathyroid hormone, although stimulation by sodium azide was present. Incubation of muscles with added parathyroid hormone produced a diminished responsiveness towards epinephrine or serotonin regulation of amino acid release and cAMP formation in the presence compared to the absence of parathyroid hormone. In the absence of parathyroid hormone, detectable inhibition of alanine and glutamine release was produced by 10(-9) M epinephrine, whereas in the presence of parathyroid hormone (1,000 ng/ml) inhibition of alanine and glutamine release required 10(-6) M or greater epinephrine. Resistance to cyclic AMP action as well as inhibition of cyclic AMP formation by parathyroid hormone was found. Preincubation of rat sarcolemma with 1-34 parathyroid hormone produced a decreased activity of the isoproterenol-stimulable adenylyl cyclase activity but there was no apparent change in the concentration of isoproterenol required for one-half maximal and maximal stimulation of the enzyme. These findings suggest that high levels of parathyroid hormone have direct effects on skeletal muscle protein, amino acid, and cyclic nucleotide metabolism in muscle of normal but not uremic animals. Treatment with these high levels of parathyroid hormone in vitro appears to reproduce in normal muscle, the metabolic deficits and loss of hormone responsiveness observed in muscle of chronically uremic animals. It is therefore possible that direct effects of parathyroid hormone on skeletal muscle may account in part for the muscle dysfunction and wasting of primary hyperparathyroidism and chronic uremia.

Adenylyl Cyclases↗
PubMed1987

Dimethyl sulfoxide increases cytoplasmic Ca2+ concentration and inhibits parathyroid hormone release in normal bovine and pathological human parathyroid cells.

The acute effects of dimethyl sulfoxide (DMSO) on parathyroid hormone (PTH) release and the cytoplasmic Ca2+ concentration (Ca2+i) were studied in dispersed bovine cells and cells isolated from human parathyroid adenomas. At extracellular Ca2+ concentrations in the 0.5-3.0 mM range, but not at less than 25 nM, addition of 2% DMSO caused a rapid rise of Ca2+i. This effect corresponded to an inhibition of PTH release and there was a strong negative correlation between Ca2+i and secretion. The actions of DMSO on Ca2+i and PTH release were less pronounced in the pathological human cells. The data are consistent with a DMSO effect on the Ca2+-sensor function of the parathyroid cell, possibly mediated by an altered plasma membrane fluidity.

Adenoma↗
PubMed1999

[Intraoperative blood sampling for parathyroid hormone measurement during total parathyroidectomy and autotransplantation in patients with renal hyperparathyroidism].

Normalisation of intact parathyroid hormone serum level confirms sufficient resection of parathyroid tissue after total parathyroidectomy in patients with secondary hyperparathyroidism. The short half-life of the intact parathyroid hormone is such that complete resection may even be confirmed by intraoperative monitoring of the hormone, and operative exploration thus reduced. We tested intact parathyroid hormone serum levels in 9 patients during total parathyroidectomy, preoperatively, after the removal of each gland, after autotransplantation and 1 month postoperatively. The serum levels of the intact parathyroid hormone were significantly reduced after removal of each gland. The total percentage decrement after parathyroidectomy with autotransplantation was 77%. However intact parathyroid hormone levels had normalised in all patients one month after the operation. The absence of perioperative normalisation of intact parathyroid hormone serum levels in our patients cannot be defined as a predictor of incomplete resection in total parathyroidectomy. The definition of an intraoperative cut-off-level concerning the decrement of intact parathyroid hormone levels remains to be proven in further studies.

Adult↗
PubMed1979

The interrelationships among prolactin, 1,25-dihydroxyvitamin D, and parathyroid hormone in humans.

Serum PRL, parathyroid hormone (PTH), and plasma 1,25-dihydroxyvitamin D [1,25(OH)2D]concentrations were measured in 6 women and 2 men with hyperprolactinemia, 6 normal men and 7 normal women, 4 men and 4 women with primary hyperparathyroidism, and 16 men and 4 women with Ca nephrolithiasis. Plasma 1,25(OH)2D and serum parathyroid hormone (PTH) concentrations were normal in the women and men with hyperprolactinemia. In patients with primary hyperparathyroidism and elevated serum PTH, plasma 1,25(OH)2D concentrations were elevated but serum PRL levels were normal. Likewise, serum PRL levels were normal in patients with Ca nephrolithiasis who had significantly elevated plasma, 1,25(OH)2D concentrations and normal serum PTH concentrations. Thus, hyperprolactinemia due to pituitary adenoma or idiopathic hypersecretion is not accompanied but elevated plasma concentrations of 1,25(OH)2D.

Adenoma↗
PubMed2000

Functional parathyroid hormone receptors are present in an umbilical vein endothelial cell line.

Acute parathyroid hormone exposure induces vascular smooth muscle relaxation. In contrast, continuous infusion of parathyroid hormone leads to vasoconstriction and an elevation of blood pressure. Despite the known effects of parathyroid hormone on vascular smooth muscle, possible direct effects on the vascular endothelium have not previously been investigated. Using a human umbilical vein endothelial cell line, we found that parathyroid hormone increased both intracellular calcium and cellular cAMP content in these endothelial cells. Furthermore, exposure of these cells to increasing concentrations of parathyroid hormone stimulated both [(3)H]thymidine incorporation and endothelin-1 secretion. Parathyroid hormone/parathyroid hormone-related peptide receptor mRNA could be detected at low levels in these cells. In summary, these data demonstrate that endothelium-derived cells contain functional parathyroid hormone receptors. The potential physiological role of these receptors remains to be determined.

Calcium↗
PubMed1975

Selective proteolysis of the receptor for parathyroid hormone in renal cortex.

Studies were carried out to determine if the receptors for parathyroid hormone, calcitonin, and prostaglandin E1 could be differentiated in renal cortex. Slices of rabbit renal cortex were incubated in buffer containing theophylline for 1 hr and then in fresh buffer with and without hormone for an additional period of 15 to 30 min. Parathyroid hormone caused a marked increase in 3',5'-AMP in both the tissue and the reaction medium. The maximal increase in 3',5'-AMP in response to prostaglandin E1 was similar to that of parathyroid hormone in the tissue but significantly less in the medium. The maximal response to calcitonin was less in both the tissue and the medium. Addition of 200 mug/ml trypsin to the first incubation abolished the subsequent response to parathyroid hormone in both the tissue and the reaction medium but did not affect the basal concentration of 3',5'-AMP or the response to calcitonin or prostaglandin E1. Controls were carried out to show that the lack of response to parathyroid hormone could not be attributed to hydrolysis of the hormone by residual trypsin. Slices were also homogenized after preincubation with and without trypsin and assayed for adenylate cyclase activity. Incubation with trypsin markedly diminished the increase in enzyme activity in response to parathyroid hormone but did not alter the basal activity or the response to calcitonin or sodium fluoride. The response to prostaglandin E1 was significantly increased. Combinations of any two or the three hormones at maximal concentrations caused an additive increase in adenylate cyclase activity. The results indicate that the receptors for parathyroid hormone, calcitonin and prostaglandin E1 in renal cortex are separate and the receptor for parathyroid hormone can be selectively hydrolyzed by proteolytic digestion.

Adenylyl Cyclases↗
PubMed1986

Comparison of three parathyroid hormone assays.

The efficiency of three parathyroid hormone (PTH) assays in the diagnosis of primary hyperparathyroidism has been investigated. Two assays used commercial reagents and measured the intact hormone and middle region of parathyroid hormone and the third assay employed the antiserum AS 211/32. Although the intact and mid-molecule assays showed a greater increase in PTH above normal than the laboratory PTH assay, patients with proven primary hyperparathyroidism were not distinguished from healthy subjects in every case. The intact and in house assays gave elevated values in seven out of nine patients with proven hyperparathyroidism and the mid-molecule assay in eight out of nine assays. The intact PTH and in-house assays were more successful than the mid-molecule method in separating patients with primary hyperparathyroidism from those with hypercalcaemia due to malignancy.

Adult↗