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PubMed1996

Effect of parathyroid hormone on renal calbindin-D28k.

The present investigation was conducted to examine the effects of parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP) on renal calbindin-D28k in rats. Four groups of studies were performed: (1) parathyroidectomy (PTX) or a sham operation followed by infusion of 1,25-dihydroxyvitamin D (1,25[OH]2D) or vehicle; (2) infusions of PTH(1-34), PTH(1-84), 1,25(OH)2D, or vehicle; (3) infusion of PTHrP(1-34), PTHrP (1-86), PTH(1-34), or vehicle; and (4) injections of calcium or vehicle. PTX reduced renal calbindin-D28k levels even when plasma concentrations of 1,25(OH)2D were kept constant by infusion of 1,25(OH)2D. Infusions of PTH(1-34), PTH(1-84), and 1,25(OH)2D all increased renal calbindin-D28k and plasma calcium, whereas PTHrP(1-34) and PTHrP(1-86) increased renal calbindin-D28k before an increase of plasma calcium took place. Hypercalcemia induced by the injection of calcium did not affect the levels of renal calbindin-D28k. The present data suggest that PTH and PTHrP exert a direct effect on renal calbindin-D28k, which is not mediated by changes of 1,25(OH)2D or calcium.

Animals↗
PubMed1976

Acquired resistance to parathyroid hormone.

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 gourth time. Serum from the patient contained antibodies of the gamma G 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.

Adenylyl Cyclases↗
PubMed2002

Parathyroid hormone regulation of type II sodium-phosphate cotransporters is dependent on an A kinase anchoring protein.

Parathyroid hormone inhibits sodium-phosphate cotransport in proximal renal tubule cells through activation of several kinases. We tested the hypothesis that the activity of these kinases was coordinated by an A kinase anchoring protein (AKAP) by demonstrating that the type II sodium-phosphate cotransporter (NaPi-4) physically associated with an AKAP and that this association was necessary for regulation of phosphate transport by parathyroid hormone. Immunoprecipitation with anti-NaPi-4 antiserum and glutathione S-transferase pull-down with GST-NaPi-4 showed that NaPi-4 associated with AKAP79, protein kinase A catalytic and regulatory subunits, and the parathyroid hormone receptor in opossum kidney cells. When the regulatory subunit of protein kinase A was uncoupled from the AKAP by a competing peptide, parathyroid hormone lost the ability to inhibit phosphate transport. This result was confirmed by co-transfecting HEK293 cells with the sodium-phosphate cotransporter and wild type AKAP, a mutant AKAP79, or the empty vector. 8-Bromo-cAMP was able to inhibit phosphate transport in cells expressing the wild type AKAP79 but not empty vector or mutant AKAP79. We conclude that parathyroid hormone inhibits proximal renal tubule sodium-phosphate cotransport through a signaling complex dependent upon an AKAP.

A Kinase Anchor Proteins↗
PubMed1978

Comparison of the effects of calcium and magnesium on parathyroid hormone secretion rate in calves.

Parathyroid hormone (PTH) secretion rate was measured in seven calves by using a technique which involved RIA of parathyroid venous blood collected during timed intervals and measured volumetrically. Infusion of solutions of NA2EDTA and MgCl2 into the jugular vein was used to alter plasma calcium and magnesium concentrations. In four calves, elevation of plasma magnesium concentration rapidly decreased the PTH secretion rate that had been stimulated by induced hypocalcemia. In three calves, equimolar and opposite changes in plasma calcium and magnesium concentrations were induced by simultaneous infusions of Na2EDTA and MgCl2. Despite the equimolar increase in plasma magnesium concentration, PTH secretion was increased in response to the decline in plasma calcium concentration. In three experiments, the concentration of each cation was kept constant during periods in which the concentration of the other cation was varied. The effect of variations in plasma magnesium concentration on PTH secretion rate was approximately 1/3-1/2 as great as that observed with changes in plasma calcium concentration. These observations indicate that the effect of magnesium on PTH secretion rate is similar to that of calcium, but not equipotent.

Animals↗
PubMed1980

Parathyroid hormone- and deoxycorticosterone acetate-induced hypertension in the rat.

1. Hypertension induced by treatment with deoxycorticosterone acetate and sodium chloride was studied in male Sprague-Dawley rats and related to parathyroid hormone secretion. 2. Lack of parathyroid hormone (due to parathyroidectomy) or decreased parathormone secretion (due to a high-calcium diet) partially inhibited the development of arterial hypertension. 3. In contrast, in thyroparathyroidectomized rats supplemented with thyroxine, the administration of parathyroid hormone rapidly elevated arterial blood pressure. 4. Maintaining a physiological concentration of serum calcium in the absence of parathyroid hormone (by feeding a high-calcium diet to parathyroidectomized rats) was not sufficient to establish mineralocorticoid hypertension. 5. These results show that parathyroid hormone is necessary for the complete development of mineralocorticoid hypertension.

Animals↗
PubMed1971

Modulation of experimental renal dysfunction of hereditary fructose intolerance by circulating parathyroid hormone.

In a woman with hereditary fructose intolerance and intact parathyroid function, the experimental administration of fructose at different dosage schedules invariably induced the dose-dependent, complex dysfunction of the proximal renal tubule now recognized as characteristic. But in a woman with hereditary fructose intolerance and hypoparathyroidism given similar amounts of fructose, the experimental dysfunction was strikingly attenuated or nondemonstrable unless or until fructose and parathyroid hormone were administered in sustained combination. Thereupon, a renal dysfunction of characteristic type and severity occurred invariably and almost immediately. Thus, the concentration of circulating parathyroid hormone can modulate the functional expression of the experimental renal disorder. This effect of parathyroid hormone, which appears to involve more than simple physiologic summation, may have important clinical implications.

Adult↗
PubMed1991

Effect of parathyroid hormone on release of interleukin 1 and interleukin 6 from cultured mouse osteoblastic cells.

This study was undertaken to examine the possibility that parathyroid hormone promotes the production of interleukin 1 and 6 in MC3T3-E1 osteoblastic cells derived from mouse calvaria. The cells were incubated in serum-free medium with or without synthetic human parathyroid hormone(1-34). The concentrations of interleukin 1 and 6 in the culture medium were determined by using specific bioassay. The cells cultured without parathyroid hormone for 24 hr released both of interleukins, and parathyroid hormone stimulated the release in a dose-dependent manner. When the cells were cultured with 10(-6) M parathyroid hormone, the release of both interleukins from the cells remained higher than control up to 144 hr. These results suggest that interleukin 1 and 6 release stimulated by parathyroid hormone may be involved in the bone resorbing activity of the hormone.

Animals↗
PubMed1976

Anabolic effect of low doses of a fragment of human parathyroid hormone on the skeleton in postmenopausal osteoporosis.

Parathyroid hormone, injected daily in low dosage, exerted anabolic effects on the human skeleton, just as it does in the rat. Four postmenopausal women with primary osteoporosis were treated for six months with a synthetic fragment of human parathyroid hormone (hP.T.H. 1-34), given as a daily injection of 100 mug. This treatment caused a remarkable acceleration of bone turnover, indicated both by isotopic tracer and histological methods. At this normocalcaemic dose level, the increases in bone formation outweighed increases in resorption. Three of the four patients showed more positive calcium balances, and mean increases in calcium and phosphorus balances were statistically significant for the group as a whole, the changes being principally due to increased intestinal absorption of both elements. Many modifications of the present method of hormone administration are possible which could further increase the preponderance of anabolic effects. These results suggest that low doses of hP.T.H. 1-34, alone or in combination with other agents, may prove useful in the treatment of osteoporosis.

Absorption↗
PubMed2000

[Diagnosis of parathyroid cysts: value of parathyroid hormone level in puncture fluid].

OBJECTIVE: Determine a means of establishing the diagnosis of parathyroid cysts preoperatively. PATIENTS AND METHODS: Classically, crystal-clear watery fluid removed by fine-needle aspiration of a suspected thyroid mass raises the suspicion of a parathyroid cyst. Immunoradiometric assay of parathyroid hormone level in the fluid may give the diagnosis sparing unnecessary surgery. RESULTS: Over the last 5 years, among the 12 patients presenting a suspected thyroid cyst containing a crystal-clear fluid, we were able to diagnose 3 cases of parathyroid cysts due to the considerable elevation of parathyroid hormone in the puncture fluid. None of these patients had hyperparathyroidism. In patients with a thyroid cyst, parathyroid hormone level in the puncture fluid was nil. CONCLUSION: The parathyroid nature of cervical cysts containing crystal-clear fluid can be established by assaying parathyroid hormone in the puncture fluid. Non-functional parathyroid cysts may be treated by repeated aspiration. Serum calcium level must be checked regularly to detect potential hyperparathryoidism.

Adult↗
PubMed1992

Parathyroid hormone responses to marked hypocalcemia in infants and young children undergoing repair of congenital heart disease.

OBJECTIVES: The integrity of the parathyroid axis was tested in 18 infants and young children undergoing repair of congenital heart disease with cardiopulmonary bypass. BACKGROUND: Infants are believed to have an immature parathyroid hormone response to hypocalcemia. Whereas adults are known to respond appropriately to hypocalcemia during cardiopulmonary bypass, children have not been studied carefully. METHODS: Calcium, magnesium, parathyroid hormone, phosphate and total protein were measured in blood samples withdrawn at defined times before, during and after cardiopulmonary bypass. RESULTS: At the initiation of cardiopulmonary bypass, ionized calcium decreased markedly in 12 infants less than or equal to 24 months old (mean +/- SEM 1.11 +/- 0.04 to 0.29 +/- 0.05 mM) and decreased significantly in 6 young children greater than 24 months old (1.19 +/- 0.02 to 0.42 +/- 0.12 mM). In response to hypocalcemia, parathyroid hormone concentration increased significantly in both the infants (from 42 +/- 8 to 103 +/- 29 and 85 +/- 22 pg/ml) and the young children (from 39 +/- 8 to 44 +/- 20 and 92 +/- 30 pg/ml). Before separation from cardiopulmonary bypass, increased parathyroid hormone concentration restored ionized calcium concentration to 0.75 +/- 0.03 mM in the infants and to 0.92 +/- 0.07 mM in the young children. There was no significant influence of either age or the use of deep hypothermia and circulatory arrest on either calcium or parathyroid hormone responses. Total magnesium and total protein concentrations decreased on initiation of cardiopulmonary bypass and thereafter remained stable. Phosphate concentrations were unchanged during the study. CONCLUSIONS: In infants and young children undergoing cardiac surgery, the parathyroid hormone response to both hypocalcemia and to rising ionized calcium concentrations was at least as great as that of adults. Thus, the calcium-parathyroid-vitamin D axis functions in infants and young children as it does in adults.

Blood Proteins↗
PubMed1995

Parathyroid hormone action in calcium transport in the distal nephron.

Urinary calcium excretion is regulated homeostatically. Regulation is achieved, in part, by the action of parathyroid hormone on Ca2+ absorption in the distal nephron. Parathyroid hormone increases Ca2+ absorption in the cortical portion of the thick ascending limb of Henle's loop in all species studied, in the murine distal convoluted tubule, and in the rabbit connecting tubule. All of these sites contain parathyroid hormone-stimulated adenylate cyclase. Both cellular and paracellular pathways of Ca2+ absorption are regulated by parathyroid hormone in the cortical portion of the thick ascending limb of Henle's loop. In both distal convoluted and connecting tubule cells, parathyroid hormone regulates transcellular Ca2+ absorption by controlling the insertion and open probability of luminal plasmalemmal Ca2+ ion channels. These channels are stimulated and inhibited by L-type calcium channel agonists and antagonists, respectively, but differ from similar channels in excitable cells in that membrane depolarization does not activate them. Parathyroid hormone also increases the driving force for diffusional Ca2+ ion entry from the luminal fluid into the cytosol by increasing the intracellular negative electrical potential (at least in murine distal convoluted tubule cells) by increasing the chloride ion conductance of the basolateral cell membrane. The effects of parathyroid hormone on the other components of cellular Ca2+ transport, via both protein kinases A and C and their interactions, remain to be examined.

Animals↗
PubMed2000

Influence of parathyroid hormone, calcitonin, 1,25(OH)2 cholecalciferol, calcium, and the calcium ionophore A23187 on erythrocyte morphology and blood viscosity.

Parathyroid hormone and calcitonin, both endocrine modulators of calcium homeostasis, may influence blood rheology. Parathyroid hormone is known to reduce erythrocyte survival, leading to anemia. Calcitonin has been found to have some vascular effects. We have analyzed the Influence of parathyroid hormone (10(-7) to 10(-10) mol/L), calcitonin (10(-6) to 10(-12) mol/L), 1,25(OH)2 cholecalciferol (10(-7) to 10(-10) mol/L), additional calcium in plasma (+1 and 2 mmol/L), and the calcium lonophore A23187 (50 micromol/L) on erythrocyte morphology and blood viscosity at high shear rate (94 s(-1)) and low shear rate (0.1 s(-1)) in vitro. The loading of erythrocytes with calcium by the ionophore A23187 produced a marked echinocytic shape transformation, an increased blood viscosity at high shear rate caused by decreased deformability of these cells, and a decreased viscosity at low shear rate caused by decreased aggregation of echinocytes. In contrast, increasing plasma calcium concentrations, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3 had no effect on erythrocyte morphology and blood viscosity. We conclude that an increase in intraerythrocytic calcium leads to severe echinocytosis and altered blood viscosity. The endocrine modulators of calcium homeostasis--namely, parathyroid hormone, calcitonin, and 1,25(OH)2 vitamin D3--apparently do not influence intraerythrocytic calcium to a significant degree and have, therefore, no influence on cell morphology and blood viscosity.

Blood Viscosity↗
PubMed1989

Trypsinization of bovine parathyroid cells abolishes Ca2+-regulated parathyroid hormone secretion.

The secretion of parathyroid hormone (PTH) is inversely related to the extracellular Ca2+ concentration (Ca2e+). To test the hypothesis that a Ca2+ sensor on the surface of parathyroid cells is involved in Ca2+-regulated PTH secretion, limited trypsinization of bovine parathyroid cells was carried out. Treatment with trypsin (1.1-10 mg/ml) inhibited, in a dose-dependent manner, PTH secretion stimulated by lowering Ca2e+ from 2.0 to 0.5 mmol/l. In control cells, activation of protein kinase C with 12-O-tetradecanoylphorbol-13-acetate (TPA) enhanced PTH secretion at 2.0 mmol Ca2e+/l but not at 0.5 mmol Ca2e+/l. In trypsinized cells, however, TPA enhanced PTH secretion at both 0.5 and 2.0 mmol Ca2e+/l. Isoproterenol-stimulated PTH secretion was maintained in trypsinized cells, but reduced cyclic AMP production revealed that some beta-adrenergic receptors were destroyed. The cytosolic free Ca2+ concentration (Ca2i+), as measured with fura-2, was raised within seconds in response to increasing Ca2e+ from 0.5 to 2.0 mmol/l and was then lowered within 1 min to a sustained plateau; the changes were the same in trypsinized and control cells. In conclusion, trypsinization of parathyroid cells abolished Ca2+-regulated PTH secretion without affecting Ca2i+.

Animals↗
PubMed1983

Large scale screening programme for selection of antisera for radioimmunoassay of human parathyroid hormone.

A large-scale, three-phase screening programme has been devised for the rapid selection of antisera which might be of potential use in clinical radioimmunoassays for human parathyroid hormone. A total of 122 sera from 169 guinea pigs and 6 rabbits immunized with bovine parathyroid hormone, and 12 guinea pigs immunized with human parathyroid hormone were assessed relative to reference antisera. Pre-determined criteria for the three phase programme were imposed by the requirement for antisera that could be used at dilutions greater than 10(-5) in order to ensure continuity of supplies for wide-spread distribution and by the limited availability of human parathyroid hormone for testing purposes. Of the sera tested, only 5 were selected as having high titre and sensitivity for low concentrations of human parathyroid hormone. The 5 antisera were further evaluated for amino- and carboxyl-region specificities for the human parathyroid hormone in comparison with antiserum 211/32, widely distributed for use in radioimmunoassay for clinical purposes. The selected antisera appear to be of high affinity with good recognition of the whole or carboxyl-region parts of the human parathyroid molecule.

Animals↗
PubMed2004

In vivo assessment of intact parathyroid hormone adsorption by different dialysis membranes during hemodialysis.

BACKGROUND: Different parathyroid hormone (PTH) behavior during hemodialysis with different types of dialysis membranes has been reported. The behavior of intact parathyroid hormone (iPTH) adsorption using different dialysis membranes was assessed in 12 dialysis patients with secondary hyperparathyroidism. METHODS: The study was performed according to a longitudinal scheme comprising three treatment modalities, each lasting 2 weeks, for 6 weeks altogether. The first treatment consisted of standard bicarbonate dialysis with low-flux polysulfone, followed by acetate-free biofiltration with high-flux-polysulfone or with polyacrylonitrile-AN69. In the first week of each period, dialysis was delivered by using a 1.3 m(2) surface area and subsequently, a 1.8 m(2) surface area. Intact parathyroid hormone was assayed on the blood and dialysate samples to calculate iPTH adsorption. RESULTS: The results showed that polyacrylonitrile-AN69 and high-flux polysulfone induce a significantly larger drop in PTH serum levels as compared with low-flux-polysulfone, particularly in the first half of the dialysis session, while the ionized calcium increase is comparable in all different hemodialysis treatments. The measurement of iPTH in the dialysate showed lower values than those disappearing on the blood side, thus suggesting the presence of an adsorptive mechanism in the different dialysis membranes. CONCLUSION: High-flux polysulfone is endowed with a comparable adsorptive capacity per surface unit compared to polyacrylonitrile-AN69, although it seems to show a different behavior, as polyacrylonitrile-AN69 saturates early in the first hour of dialysis corresponding to its maximum adsorption power, while high-flux-polysulfone displays a more lasting adsorptive capacity. Thus, iPTH changes during hemodialysis also depend on dialyzer characteristics and the dialysis membrane adsorption.

Acrylic Resins↗
PubMedDate not supplied

[Regulation of in vitro metabolism of human spongiosa by parathyroid hormone and calcitonin].

A method was developed to investigate in vitro metabolism of human trabecular bone and its hormonal regulation. Human and bovine parathyroid hormone 1-34 caused an increase in the release of calcium and magnesium out of human bone. Human, salmon and porcine calcitonin caused a decrease in the release of calcium and magnesium and inhibited the effect of parathyroid hormone.

Aged↗
PubMed1999

Parathyroid hormone enhances fracture healing. A preliminary report.

This investigation tested the hypothesis that daily parenterally administered parathyroid hormone (1-34) improves fracture healing. Twenty, 3-month-old, male Sprague Dawley rats weighing approximately 400 g each, underwent the production of closed, unilateral mid-diaphyseal femoral fractures. Animals were divided into two groups of 10; the animals received either a daily subcutaneous injection of delivery vehicle (0.9% saline) or 80 micrograms/kg parathyroid hormone. On Day 21 after fracture the animals were euthanized, the femurs were removed and subjected to biomechanical testing, bone densitometry (dual energy x-ray absorptiometry, peripheral quantitative computed tomography), and histologic examination. Treatment with parathyroid hormone resulted in statistically significant increases in callus area and strength. Histologic examination of the calluses showed an increase in the amount of new bone formed. No differences were observed in the weights of the animals or the sizes of the bones. Values obtained using dual energy x-ray absorptiometry and peripheral quantitative computed tomography indicate an increase in density in the parathyroid hormone treated fractures consistent with the histologic appearance and the findings of increased strength, although these bone density changes did not achieve statistical significance. These results suggest that parenterally administered parathyroid hormone (1-34) may enhance or accelerate normal fracture healing and support the concept that this hormone be tested clinically as a systemic treatment for fractures that are slow to heal.

Absorptiometry, Photon↗
PubMed1983

Restoration of phosphaturia in phosphate-deprived rats in the presence of both parathyroid hormone and phosphate infusion.

The present study tested the hypothesis that the combination of parathyroid hormone and phosphate infusion would be phosphaturic in phosphate-deprived rats. Clearance experiments were performed in Sprague-Dawley rats fed a low-phosphate diet for 4 days. The animals were first given a phosphate infusion and then administered parathyroid hormone. The reverse experiment was also performed in a second group of rats by giving the hormone first followed by a phosphate infusion. There was no increase in phosphate excretion in response to phosphate infusion or parathyroid hormone given alone. However, the combination of parathyroid hormone and phosphate infusions, given in either order, was phosphaturic in phosphate-deprived rats.

Animals↗