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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↗
PubMedDate not supplied

Hormone metabolism and response of adenylate cyclase to parathyroid hormone in kidney.

1. Incubation of parathyroid hormone with plasma membranes from rat kidney cortex resulted in rapid loss of all hormal activity. 2. Chick kidney membranes showed no ability to inactivate parathyroid hormone even with prolonged incubation. 3. Biologically active, labelled parathyroid hormone was degraded to fragments by rat kidney membranes, but not by chick kidney. 4. Hormone-responsive adenylate cyclase activity in a mixture of rat and chick kidney membranes was additive. 5. Parathyroid hormone bound specifically to chick kidney palsma membranes. 6. It is concluded that hormone in activation during incubation has little relevance to the effectiveness of parathyroid hormone in stimulating adenylate cyclase activity in kidney, and furthermore that failure of chick kidney to metabolize the hormone is not the explanation for the greater sensitivity of this species to the hormone.

Adenylyl Cyclases↗
PubMed1976

Impaired release of parathyroid hormone in magnesium deficiency.

Parathyroid hormone release and end-organ responsiveness to parathyroid extract (PTE) were evaluated in a 25-year-old woman with magnesium deficiency associated with hypocalcemia and inappropriately low levels of serum immunoreactive parathyroid hormone (iPTH). End-organ responsiveness to PTE was demonstrated by increases in serum calcium and in urinary phosphorus, cyclic AMP, and hydroxyproline. When the serum calcium was increased from a baseline of 6.9 mg/100 ml to levels of 8.0 mg/100 ml and higher by calcium infusion, the serum iPTH decreased from the low normal range to below the limits of detectability. The intravenous administration of 3 mg/kg of body weight of magnesium led to an abrupt and striking increase in circulating iPTH with a 2-fold increase in one minute, a 6-fold increase in two minutes, and an 8-fold increase in five minutes. The very rapid increase in serum iPTH produced by magnesium infusion in this study suggests an effect of magnesium on hormone secretion rather than an effect on hormone synthesis. The evidence provided by this investigation indicates that the release of parathyroid hormone is impaired in magnesium deficiency and that the level of circulating calcium required for the suppression of parathyroid hormone secretion is lower than that in normal subjects.

Adult↗
PubMed1997

Control of hair growth with parathyroid hormone (7-34).

Parathyroid hormone (PTH) related peptide (PTHrP) is thought to influence the proliferation and differentiation of the epidermis and hair follicle. As a means of elucidating the biologic function of PTHrP on the hair follicle, a PTHrP analog PTH (7-34), which is a PTH/PTHrP receptor antagonist, was given intraperitoneally twice daily to C57 BL/6 mice at different stages of the hair cycle. PTH (7-34) induced 99 +/- 4.5% (mean +/- SEM) of resting telogen hair follicles into a proliferative (anagen) state, whereas 100% of the hair follicles in the control group remained in telogen. To determine whether this peptide influenced the progression of the hair follicles from anagen to catagen (hair follicle maturation and regression), groups of mice that were either spontaneously in or induced to anagen received either PTH (7-34) or placebo. Morphometric analysis of the hair follicles from the middle back region of the spontaneous anagen mice that received PTH (7-34) revealed that 19 +/- 4% (mean +/- SEM) of the follicles were in anagen VI, whereas none (0%) were in anagen in the control group. Similarly, in induced anagen mice treated with PTH (7-34), 22.3 +/- 1.4 (mean +/- SEM) of the follicles were in anagen VI compared to only 1.3 +/- 0.7% in the control mice. Together these observations suggest that PTHrP is a hair follicle morphogen that may be a major factor responsible for controlling the hair cycle. These studies provide a new insight for development of PTHrP analogs for a wide variety of disorders related to disturbances of hair cycling.

Animals↗
PubMed1989

Molecular cloning and chromosomal mapping of DNA rearranged with the parathyroid hormone gene in a parathyroid adenoma.

Parathyroid adenomas are common benign neoplasms for which no chromosomal defects have been described. We recently found two parathyroid adenomas bearing clonal restriction fragment abnormalities involving the PTH locus, and now show that in one of these tumors: (a) a DNA rearrangement occurred at the PTH locus; (b) the rearrangement separated the PTH gene's 5' flanking region from its coding exons, conceivably placing a newly adjacent gene under the influence of PTH regulatory elements; (c) the DNA that recombined with PTH normally maps to 11q13, the known chromosomal location of several oncogenes and the gene for multiple endocrine neoplasia type I; and (d) the rearrangement was a reciprocal, conservative recombination of the locus on 11q13 (Human Gene Mapping Library assignment D11S287) with PTH (on 11p15). These data provide molecular cytogenetic evidence for the clonal occurrence of a major chromosome 11 aberrancy in this benign parathyroid tumor. The D11S287 clone could prove useful in genetic linkage analyses, in determining precise 11q13 breakpoints in other neoplasms, and in identifying a gene on chromosome 11 that may participate in parathyroid tumor development.

Adenoma↗
PubMed1989

Calcium-dependent release of N-terminal fragments and intact immunoreactive parathyroid hormone by human pathological parathyroid tissue in vitro.

The regulation of PTH secretion by extracellular calcium was studied in parathyroid tissue obtained from patients with hyperparathyroidism (adenoma or hyperplasia) using both an amino (N)-terminal RIA as well as an immunoradiometric assay (intact assay) specific for the intact hormone. The parathyroid glands separated into three major groups when examined in terms of absolute amounts of PTH secreted, degree of suppressibility, and set-point for calcium (the concentration of calcium causing half-maximal inhibition of PTH release). In cell preparations from group A (two different adenomas, two hyperplastic glands from a patient with renal failure, and a hyperplastic gland from a patient with hypophosphatemic rickets), both assays showed comparable PTH release (agreeing within 2-fold), similar degrees of suppressibility and similar, if not identical, set-points. In group B (two adenomas and one hyperplastic gland from a patient with renal failure), PTH secretion, as measured in the N-terminal assay, was 3- to 6-fold more than that measured in the intact assay. The set-points and maximal degrees of suppressibility were, however, still comparable. In group C [two adenomas and one gland from a patient with hypophosphatemic rickets (the sister of the patient in group A)], no suppressibility was observed when PTH release was measured using the intact assay (i.e. less than 50% suppression of PTH release at 2-3 mM Ca2+). In one of these three glands, the N-terminal assay was used in addition to the intact assay, and no suppressibility was present with either assay. Thus, in general, the effects of extracellular Ca2+ on PTH secretion from pathological parathyroid tissue were similar when assessed with both an N-terminal and an intact assay, at least with respect to setpoint and maximal suppressibility. In a few cases, maximal PTH release was greater when measured with the N-terminal assay, consistent with substantial release of N-terminal fragments in addition to intact PTH. In addition, nonsuppressible glands were not uncommon when PTH release was measured by the intact assay, confirming previous studies with less specific assays.

Adolescent↗
PubMed1996

Persistent elevated serum levels of intact parathyroid hormone after operation for sporadic parathyroid adenoma: evidence of detrimental effects of severe parathyroid disease.

BACKGROUND: A significant number of patients with primary hyperparathyroidism (pHPT) who are surgically treated have increased serum levels of intact parathyroid hormone (PTH) during long-term follow-up despite normocalcemia. The cause and significance of this finding remain to be established. METHODS: A total of 82 patients operated on for sporadic parathyroid adenoma were investigated before and at 8 weeks and 1 year after operation with serum levels of intact PTH, bone mineral content, and biochemical variables known to reflect PTH activity. RESULTS: All patients had low or normal serum levels of calcium during follow-up. At 8 weeks after operation 20 (24%) patients had increased serum levels of PTH. These patients had severe parathyroid disease and low levels of 25(OH) vitamin D before operation. In contrast to patients with normal levels of PTH after operation, they did not have an elevated bone mineral content but had elevated levels of serum creatinin. At 1 year after operation 13 patients had elevated serum levels of PTH. Compared with patients with normal serum levels of PTH, they were older and had an increased frequency of cardiovascular disease and biochemical indications of compromised renal function. They did not have an elevated bone mineral content. CONCLUSIONS: Persistently increased serum levels of PTH indicate harmful effects of pHPT even after surgical cure, especially in elderly patients with severe disease before operation. The results in this investigation therefore favor early treatment of pHPT.

Adenoma↗
PubMed1987

The effect of vincristine on parathyroid hormone release and on the parathyroid cell microtubular structures in the intact rat.

The effect of vincristine on immunoreactive parathyroid hormone (iPTH) release and parathyroid cell microtubular structures was evaluated in intact, unanaesthetized, and unrestrained rats with indwelling catheters. In overnight fasted rats, blood samples were collected before and at 30, 60 and 120 min after iv vincristine administration in low dosage (0.15 mg/kg) or in higher dosage (0.5 mg/kg) or vehicle (controls) for serum iPTH and calcium determinations. Mean baseline serum iPTH and calcium concentrations were similar in the vincristine-treated and the control rat. Following the low dose vincristine treatment, serum iPTH slightly but significantly declined to 89 +/- 5% at 30 min and remained at this low level at 60 and 120 min as compared to those observed in control rat. Similarly, iPTH concentrations after higher doses of vincristine were also significantly decreased to 87 +/- 4% at 30 min and to 83 +/- 4% at 60 min, and 86 +/- 7% at 120 min as compared to those observed in the control rat. Serum calcium concentrations were similar in the vincristine-treated and control rats. In the next study, each of the rats received vincristine and vehicle in a random order, 10 days apart. In this study also, mean serum iPTH significantly declined to 85 +/- 7% at 60 and 120 min during vincristine treatment as compared with those observed during the vehicle treatment in the same rats. Parathyroid glands were removed from rats between 60 and 120 min after vincristine or vehicle treatments for electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Parathyroid hormone: regulation of synthesis and secretion.

Calcium homeostasis is essential for survival and is primarily achieved through the actions of parathyroid hormone. Parathyroid hormone secretion and synthesis are primarily regulated by serum calcium levels, although other factors such as vitamin D and neurotransmitters play a role. This review is intended to provide the reader with up to date information on the current state of basic cell regulation research into parathyroid function. While some mention of disease states is made, the focus of this review is on the calcium regulation of parathyroid hormone secretion at the molecular level. Individual sections will discuss calcium-sensing, signal transduction by calcium and other secretagogues, regulation of parathyroid hormone synthesis, and strategies of regulation of parathyroid hormone secretion by calcium. Particular emphasis is given to the calcium-stimulated degradation of parathyroid hormone within the parathyroid as one of the major pathways by which circulating levels of bioactive hormone are controlled.

Amino Acid Sequence↗
PubMed1997

[Cushing's syndrome due to small cell lung cancer with ectopic production of adrenocorticotropic and parathyroid hormone].

A 72-year-old man was admitted to our hospital because of a tumor-like shadow on a chest X-ray film. At the initial examination, he had clinical signs of Cushing's syndrome: moon face, central obesity, and hypertension. A computed tomographic scan of chest showed an abnormal shadow in the lung (5 x 6 cm) with involvement of the right paratracheal and anterior tracheal lymph nodes, and a right-sided pleural effusion. Small cell lung cancer (extended disease; T2N2M6 stage IV) was diagnosed after a transbronchial biopsy. The concentrations of adrenocorticotropic hormone, cortisol, and parathyroid hormone in plasma were markedly elevated, and there was no circadian rhythm (336 pg/ml. more than 60.1 micrograms ml. and 805 pg/ml, respectively). Fluid obtained by thoracentasis had malignant cells, and the levels of adrenocorticotropic hormone and parathyroid hormone in the effusion (1120 pg/ml and 1810 pg/ml, respectively) were higher than those in serum, which indicates that these hormones were produced by the tumor cells. The patient received chemotherapy and responded well, but he died of respiratory failure 26 months later. The response rate to chemotherapy in elderly patients with lung cancer is said to be comparable to that in younger patients, but treatment may be difficult because of poor performance status and diminished physical capacity. Although patients with lung cancer complicated by Cushing's syndrome have a poor prognosis, this patient survived for more than 2 years after the disease was diagnosed.

Adrenal Cortex Hormones↗
PubMed1997

Comparison of the abilities of human parathyroid hormone(1-31)NH2 and human parathyroid hormone-related protein(1-31)NH2 to stimulate femoral trabecular bone growth in ovariectomized rats.

N-terminal fragments of PTH and PTHrP, such as hPTH-(1-34) and hPTHrP-(1-34), are sufficiently similar with respect to amino acid sequence, location of functional domains, and higher order configuration to activate the same PTH/PTHrP receptor and the same two signal enzymes, adenylyl cyclase and phospholipase-Cbeta. Therefore, it was expected that hPTHrP-(1-31)NH2 would stimulate bone growth in ovariectomized rats as strongly as hPTH-(1-31)NH2. Like hPTH-(1-31)NH2, hPTHrP-(1-31)NH2 stimulated adenyly cyclase in ROS 17/2 osteosarcoma cells as strongly as the standard hPTH-(1-34) and like hPTH-(1-31)NH2, triggered a large drop in mean blood pressure when injected intravenously. Unlike hPTH-(1-31)NH2, however, hPTHrP-(1-31)NH2 could not stimulate trabecular growth in the distal femurs of young, sexually mature, ovariectomized rats.

Adenylyl Cyclases↗
PubMed1988

[The measurement of parathyroid hormone in sera of hemodialysis patients with renal insufficiency by employing the various kinds of parathyroid hormone kits].

This study focussed on elucidating difference of blood PTH levels, by employing the various kinds of PTH kits. We carried out the measurements of PTH levels in sera of the hemodialysis patients with renal insufficiency presumably inactivated PTH degradative regulation in kidney. Our results showed the remarkable significant relationships among blood PTH levels of carboxyl and mid-region PTH and intact PTH in hemodialysis patients and was deduced that the difference of PTH levels by using various kinds of PTH kits was responsible of PTH cleavage effect in the kidney.

Adult↗
PubMed1999

Hyperphosphatemia accelerates parathyroid cell proliferation and parathyroid hormone secretion in severe secondary parathyroid hyperplasia.

We studied the role of phosphorus retention in parathyroid cell proliferation and parathyroid hormone (PTH) oversecretion in severe secondary parathyroid hyperplasia. Mice transplanted with human parathyroid tissue from a patient who had undergone parathyroidectomy for severe secondary hyperparathyroidism were divided into four groups; each group was given a diet with a different phosphorus content (0.4, 0.7, 1.0, and 1.2%) to alter serum phosphorus concentrations. Histologic examinations of grafts by hematoxylin-eosin or by bromodeoxyuridine (BrdU) immunohistochemical staining were performed to assess parathyroid cell proliferation. Changes in serum phosphorus concentrations unidirectionally affected PTH secretion from the graft, because human PTH did not cross-react with mouse PTH. Serum phosphorus concentrations of 1.0P and 1.2P groups were significantly higher than those of 0.4P and 0.7P groups (p<0.05). Serum phosphorus concentrations were significantly correlated with the gradient of human PTH elevation with a coefficient of 0.48 and a p<0.05. Furthermore, serum phosphorus concentrations and the gradient of human PTH elevation were significantly higher in mice with BrdU-immunoreactive cells in the parathyroid graft than in mice without immunoreactive cells in the graft. These results indicate that uncontrolled hyperphosphatemia may accelerate the proliferation of parathyroid cells, exacerbating PTH oversecretion.

Animals↗