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PubMed1992

Specific binding of parathyroid hormone to living osteoclasts.

We show that osteoclasts bind parathyroid hormone (PTH) in a manner that displays the properties of receptor-dependent hormone binding, that is, saturability, time dependence, temperature dependence, and hormone specificity. Osteoclasts were isolated from the endosteum of 2 to 3 week chick tibiae and maintained in culture for 4-6 days. Bovine PTH-(1-84) was biotinylated with N-hydroxysuccinimidobiotin. Biotinyl-PTH (btPTH, 10(-5)-10(-11) M) was added to the cultured osteoclasts for 2-20 minutes. After rinsing away unbound btPTH, fluorescein isothiocyanate-labeled avidin (FITC-avidin) at a concentration of 66 micrograms/ml was applied. Receptor binding characteristics were assessed: (1) saturation occurred at around 10(-6) M btPTH; (2) competition of excess unlabeled PTH was found, namely, a 10-fold excess abolished fluorescence; (3) specificity was shown by adding other polypeptide hormones (insulin, glucagon, and calcitonin) in 10- to 100-fold excess--no effect on PTH binding was observed; and (4) affinity of btPTH for its binding site was indicated by half-maximal binding approximately equal to 10(-7) M for both osteoclasts and osteoblasts. Biotin (10(-5) M) or FITC-avidin (66 micrograms/ml) alone did not cause fluorescence. The time course of btPTH on the cell exterior was short: at 2 and 5 minutes dots of fluorescence were randomly dispersed over the cell surface, by 10 minutes most of the fluorescence was clustered in one region of the membrane, and by 20 minutes most of the hormone was no longer present on the surface of the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Avidin↗
PubMed1990

The measurement of circulating parathyroid hormone.

Until recently, the measurement of circulating parathyroid hormone (PTH) has been unsatisfactory due to poor analytical performance of immunological assays and due to interference in such assays by circulating biologically inactive fragments of PTH. The development of a two-site immunometric assay with the use of acridinium ester as label has solved these problems. This immunochemiluminometric assay (ICMA) measures the intact molecule and is capable of detecting PTH levels in normal subjects as well as suppression of PTH after oral administration of calcium. The ICMA PTH assay has been shown to be adequate in the diagnosis of primary hyperparathyroidism and it could prove useful in monitoring renal failure patients and investigating other bone diseases such as osteoporosis.

Humans↗
PubMed1985

Induction of spermidine/spermine N1-acetyltransferase by parathyroid hormone in rabbit costal chondrocytes in culture.

Parathyroid hormone (PTH) increased the activity of spermidine/spermine N1-acetyltransferase, a rate-limiting enzyme of polyamine biodegradation, in rabbit costal chondrocytes in culture. The enzyme activity increased in a dose-dependent manner after addition of PTH to the culture, reaching a maximum at 8 h. The increase in the enzyme activity was abolished by cycloheximide or actinomycin D. Dibutyryl cyclic AMP also induced the acetyltransferase to some extent. These results suggest that the induction of spermidine/spermine N1-acetyltransferase by PTH may play some significant role in the expression of the differentiated phenotype of chondrocytes.

Acetyltransferases↗
PubMed1986

Increased parathyroid hormone as a consequence of changed complex binding of plasma calcium in morbid obesity.

To evaluate whether changed plasma calcium binding might lead to a secondary increase of parathyroid hormone in morbid obesity, fasting measurements of serum ionized, ultrafiltrable and total calcium, calcium binding substances, and parathyroid hormone were undertaken in age- and sex-matched groups of obese (n = 44) and normal weight subjects (n = 52). The 24-hour urinary calcium excretion and clearance of creatine were also measured. Calcium binding to proteins was changed. Serum total proteins and protein-bound calcium did not differ, but serum albumin was decreased in obesity. Consequently, obese subjects did not reveal the normal dependency of protein-bound calcium upon albumin. Calcium binding to other substances was also changed. Serum phosphate and bicarbonate were decreased, while the concentrations of citrate, lactate, acetoacetate, 3-hydroxybutyrate, free fatty acids, and urate were all increased, leaving the total concentration of plasma complex-bound calcium unchanged. Nevertheless, these reciprocal changes increase the concentrations of less readily reabsorbable anions in the renal ultrafiltrate. The changed pattern of calcium binding in serum of the obese subjects may serve to explain our findings of increased urinary calcium excretion, lowering of serum ionized calcium and increased parathyroid hormone levels, changes being significantly correlated with degree of overweight.

Adult↗
PubMed2005

Diurnal variations in the plasma concentration of parathyroid hormone in dogs.

The plasma concentrations of parathyroid hormone (PTH), ionised calcium (Ca(2+)), total calcium, albumin and inorganic phosphorus, and the pH were measured in blood samples obtained from nine dogs during a period of 26 hours. The plasma pth levels fluctuated slightly during the day, by about 20 pg/ml, but there was a distinct peak (42.8 [8.8] pg/ml) at 07.00. Plasma Ca(2+) showed a diurnal pattern in which two peaks (increases of 0.03 mmol/l) were observed at 05.00 and 17.00, and the plasma concentration of inorganic phosphorus showed a similar pattern. There were no diurnal changes in total calcium or albumin.

Animals↗
PubMed1987

The relationship of calcium and parathyroid hormone in their effect on heart cells.

Parathyroid hormone (PTH), the plasma concentration of which is raised in uremia, has been suggested as one of the agents responsible for the myocardial changes commonly seen in uremia. The effect of intact PTH on rat heart cells grown in tissue culture has been studied. Addition of the hormone to the media significantly stimulated beating rate. The stimulation was directly proportional to the amount of PTH in the medium. Excessively high concentration of PTH caused immediate cessation of the beating, which was reversed by the addition of calcium to the medium. The extent of stimulation by PTH was inversely proportional to the calcium concentrations in the medium. Isoproterenol and phenylephrine at excessively high concentrations in the medium did not mimic the PTH effect either alone or together with PTH. When beating ceased due to verapamil the effect was not reversed by the addition of calcium to the medium. Calcium added to the myocytes seen after beating ceased reversed the effect and the cells started to beat again. Cells kept for a longer period in the arrested state were not revived by the addition of calcium.

Animals↗
PubMed1983

Semi-preparative high-performance liquid chromatographic purification of a 28-amino acid synthetic parathyroid hormone antagonist.

Structure-activity studies of parathyroid hormone (PTH) over the last decade have led to the design and synthesis of a peptide hormone inhibitor of PTH action in vivo, [Tyr-34]bPTH-(7-34)amide. To evaluate the biological properties of this 28-amino acid hormone analogue, sufficient amounts of the peptide needed to be prepared in a high state of purity to permit continuous infusion in groups of animals for periods of several hours. For this purpose, gel chromatography followed by semi-preparative, reversed-phase high-performance liquid chromatography (HPLC) using a lyophilizable solvent gradient system of acetonitrile in 0.1% trifluoroacetic acid was utilized. In a parallel purification scheme, gel filtration followed by ion-exchange chromatography was employed. Comparison of yields and product purity were determined by a battery of chemical analytical techniques. Semi-preparative HPLC generated a highly purified product; substantial heterogeneity was detected in the ion-exchange-purified material. The HPLC-purified product retains the biological activities of binding to PTH receptors in vitro and inhibiting PTH action in vivo.

Amino Acid Sequence↗
PubMed1986

Intact parathyroid hormone (1-84) in primary hypertension.

Intact parathyroid hormone (1-84) (PTH) concentrations were measured in serum of 83 hypertensive and 83 normotensive subjects, aged 20 to 69 years, matched for age and gender, and selected from the same open population. No significant differences in serum intact-PTH levels were found between the total group nor between groups based on three age strata. However, PTH was negatively associated with body weight and after adjustment for differences in body weight, significantly higher intact-PTH levels were found in hypertensive than in normotensive subjects, aged 20-39 years, but not in those aged 40 to 69 years. Our findings suggest that body weight is a confounding variable when comparing differences in intact-PTH between groups. Intact-PTH levels may be increased in a subgroup of young primary hypertensive subjects.

Adult↗
PubMed2006

The role of parathyroid hormone measurements after surgery for primary hyperparathyroidism.

BACKGROUND: During parathyroidectomy for primary hyperparathyroidism (pHPT), intraoperative parathyroid hormone (IOPTH) levels are used to confirm removal of all hyperfunctioning parathyroid tissue. The phenomenon of elevated parathyroid hormone (PTH) levels with normocalcemia after curative parathyroidectomy, seen in up to 40% of patients, continues to be an unexpected and unexplained finding. We therefore investigated whether postoperative PTH levels are as reliable as IOPTH levels in predicting cure after surgery for pHPT. METHODS: We reviewed our prospective database of consecutive patients undergoing surgery for pHPT between December 1999 and November 2004. Curative parathyroidectomy was defined as normocalcemia 6 months or longer postoperatively. RESULTS: A total of 328 patients who underwent 330 operations for pHPT had IOPTH measurements and serum follow-up calcium levels at 6 months or longer. Surgery was curative in 315 (95.5%) operations. IOPTH levels correctly predicted operative success in 98.2% (positive predictive value [PPV]. Postoperatively, the PPV of a normal PTH level at 1 week, 3 months, and 6 months was 97.1%, 97.3%, and 96.5%, respectively. Of all patients with an elevated postoperative PTH level at 1 week, 3 months, or 6 months, only 13.7%, 14.3%, and 14%, respectively, were not cured. CONCLUSIONS: Normal postoperative PTH levels reliably predict operative success. However, they do not improve upon results predicted by IOPTH levels. Elevated postoperative PTH levels do not predict operative failure in most patients. We propose that PTH measurements after surgery for pHPT may be misleading, costly, and not indicated in normocalcemic patients.

Adolescent↗
PubMed1994

The effect of long- and short-term corticosteroids on plasma calcitonin and parathyroid hormone levels.

The role of calcitonin and parathyroid hormone (PTH) in corticosteroid-induced osteoporosis is controversial. We therefore measured plasma calcitonin and PTH levels in 34 adults receiving chronic pharmacological corticosteroids for obstructive airways disease, and in controls matched for age, sex, menopause, and disease. In addition, the acute effect of a 7-day course of 15 mg prednisolone daily on fasting and calcium-stimulated calcitonin was studied in 10 normal male volunteers. There was no difference in calcitonin and PTH levels in the corticosteroid-treated patients when compared with controls. The corrected serum calcium was significantly higher in the steroid-treated patients (patients mean 2.40 (SEM 0.01) mmol/liter; controls mean 2.33 (SEM 0.01) mmol/liter; P < 0.001). The short course of corticosteroids in volunteers did not alter basal or stimulated calcitonin, PTH, or calcium levels. These results suggest that neither calcitonin deficiency nor PTH excess is a feature of corticosteroid-induced osteoporosis.

Adult↗
PubMed1994

A method for the high-level expression of a parathyroid hormone analog in Escherichia coli.

A recombinant parathyroid hormone analog, rPTH(1-34*), was obtained from Escherichia coli using a gene polymerization strategy. The PTH gene polymer contains up to 8 copies of the gene, each separated by a cleavable linker. The polymer was expressed at very high levels and formed inclusion bodies which could be easily isolated by low-speed centrifugation. A polyhistidine leader peptide allows rapid purification via nickel chelation chromatography of the PTH polymer solubilized from the inclusion bodies. Yields of greater than 500 mg/liter have been obtained. After isolating the polymer, monomeric rPTH(1-34*) is released from the polymer by chemical cleavage with cyanogen bromide. Following cyanogen bromide cleavage and high-performance liquid chromatography purification, highly purified, biologically active rPTH(1-34*) is obtained at a yield of approximately 300 mg/liter. This is a general strategy for the high-level production of a variety of peptides and small proteins.

Adenylyl Cyclases↗
PubMed2006

Impaired bone anabolic response to parathyroid hormone in Fgf2-/- and Fgf2+/- mice.

Since parathyroid hormone (PTH) increased FGF2 mRNA and protein expression in osteoblasts, and serum FGF-2 was increased in osteoporotic patients treated with PTH, we assessed whether the anabolic effect of PTH was impaired in Fgf2-/- mice. Eight-week-old Fgf2+/+ and Fgf2-/- male mice were treated with rhPTH 1-34 (80mug/kg) for 4 weeks. Micro-CT and histomorphometry demonstrated that PTH significantly increased parameters of bone formation in femurs from Fgf2+/+ mice but the changes were smaller and not significant in Fgf2-/- mice. IGF-1 was significantly reduced in serum from PTH-treated Fgf2-/- mice. DEXA analysis of femurs from Fgf2+/+, Fgf2+/-, and Fgf2-/- mice treated with rhPTH (160mug/kg) for 10 days showed that PTH significantly increased femoral BMD in Fgf2+/+ by 18%; by only 3% in Fgf2+/- mice and reduced by 3% in Fgf2-/- mice. We conclude that endogenous Fgf2 is important for maximum bone anabolic effect of PTH in mice.

Animals↗
PubMed1982

Application of newly synthesized 1-34 human parathyroid hormone for diagnostic tests.

1-34 human parathyroid hormone (1-34 hPTH) was synthesized by a liquid-phase method and prepared for clinical use (specific activity, 3281 U/mg). With this preparation, the toxicity was studied in 22 normal volunteers and the metabolic effects in 15 individuals. Intradermal administration of 4 ng of 1-34 hPTH caused neither abnormal local skin reactions nor toxicity in terms of subjective and objective parameters. When administered intravenously at doses of from 2 to 20 microgram as a bolus, the preparation caused no acute or subacute toxicity judging from the results of various clinical and laboratory studies, except for transient mild hypotension and headache in a minority of subjects. For diagnostic use, 20 microgram of 1-34 hPTH administered intravenously was found to produce effects almost equivalent to those of 200 USPU U of Parathormone (PTE, Eli Lilly). Thus, the criteria for differentiation of hypoparathyroidism from pseudo-hypoparathyroidism devised with 2000 USP U of PTE as a test substance was found to be applicable when 20 microgram of 1-34 hPTH was utilized.

Animals↗
PubMed1985

Cardiovascular responses to parathyroid hormone.

The synthetic amino terminal fragment of parathyroid hormone, PTH-(1-34), is a potent coronary artery vasodilator in the dog. In the present study, using instrumented open-chest dogs, we have performed the initial characterization of this effect and showed other dose-related cardiovascular effects of the hormone. A near-maximal flow response was obtained after intracoronary injection of 0.024 nmol X kg-1 PTH-(1-34) with minor, if any, concomitant changes in mean blood pressure, contractile force, or heart rate. At higher doses, mean blood pressure decreased while contractile force and heart rate increased in dose-dependent fashion. Infusion of PTH-(1-34) for 20 min showed that the vasodilatory effect could be sustained without a concomitant decrease in mean arterial pressure. Pharmacological characterization showed for the first time that the coronary response to PTH-(1-34) was unaltered in the presence of beta- or alpha-adrenergic, muscarinic, or histaminergic blockades. We conclude that PTH-(1-34), an endogenous circulating calcemic peptide, produces a large increase in coronary blood flow at doses sufficiently low to preclude complicating effects on blood pressure, contractile force, and heart rate. Furthermore, the results suggest that the vasodilatory effects may be specific.

Animals↗
PubMed2006

Successful minimally invasive parathyroidectomy for primary hyperparathyroidism without using intraoperative parathyroid hormone assays.

BACKGROUND: The need for intraoperative parathyroid hormone (iPTH) assays in minimally invasive parathyroidectomy (MIP) remains controversial. We report the results of MIP performed without the use of iPTH assays. METHODS: This was a single-institution retrospective review of patients with primary hyperparathyroidism treated with MIP between October 1, 1998, and December 31, 2002. RESULTS: Seventy-seven patients were studied. The mean preoperative calcium level was 11.4 mg/dL. All patients had a normal calcium level postoperatively (range, 7.4-10.2 mg/dL, mean, 9.1 mg/dL). Three patients (4%) required re-exploration for various reasons including the development of a second adenoma, secondary hyperparathyroidism, and discordant pathology. All 3 patients initially were eucalcemic. CONCLUSIONS: Our success rate of 96% using a combination of preoperative sestamibi scans, intraoperative gamma probe localization, and selective frozen pathology is consistent with the published success rates using iPTH assays of 95% to 100%. We conclude that MIP can be performed successfully without using iPTH assays.

Adolescent↗
PubMed1986

Heterologous desensitization by 1,25-dihydroxyvitamin D-3 of cyclic AMP response to parathyroid hormone in osteoblast-like cells and the role of the stimulatory guanine nucleotide regulatory protein.

The influence of 1,25-dihydroxyvitamin D-3 on the cAMP response to parathyroid hormone was studied in the osteoblast-like rat osteosarcoma cells ROS 17/2.8. The stimulation by parathyroid hormone of cAMP production in intact cells and of adenylate cyclase activity in isolated plasma membranes was attenuated by 1,25-dihydroxyvitamin D-3 treatment. This was associated with a reduction of the stimulatory guanine nucleotide regulatory protein, as demonstrated by a lower response to NaF and guanosine 5'-[beta, gamma-imido]triphosphate, and by a lower activity of solubilized plasma membrane extracts in the reconstitution assay. 1,25-dihydroxyvitamin D-3 blunted also the cAMP response to parathyroid hormone in cells incubated with the glucocorticoid dexamethasone, where a higher activity of the adenylate cyclase catalytic unit was observed. Thus, the two steroids appear to affect distinct levels of the adenylate cyclase system. Furthermore, the two hormones also showed an antagonistic effect upon the production of osteocalcin, an osteoblast-specific extracellular matrix protein. The release of this non-collagenous matrix protein by ROS 17/2.8 cells was increased by 1,25-dihydroxyvitamin D-3 and decreased by dexamethasone.

Adenylyl Cyclases↗
PubMed1983

Effect of parathyroid hormone on renin secretion.

The ability of parathyroid hormone (PTH) to increase renin secretion was investigated in pentobarbital-anesthetized dogs. An intravenous infusion of bovine PTH 1-34, at the dose of 0.028 microgram/kg-1 min-1 increased renin secretion by 149% (501 +/- 105 to 1249 +/- 309 ng hr-1 min-1); renin secretion returned to control values during the recovery period. In order to determine whether PTH acted directly on the kidney to increase renin secretion, PTH was infused into the right renal artery at doses of 0.0014 to 0.0028 microgram/kg-1 min-1 and renin secretion from the right kidney was compared to that from the left (control) kidney. Renin secretion from the right (PTH-infused) kidney was not greater than control values for that kidney or different from the renin secretory rate of the left (control) kidney. In contrast, the excretion rates of both phosphate and sodium from the right kidney were greater than control values and from the excretion rates of the left kidney. These data suggest that PTH, while acting directly on the kidney to increase phosphate and sodium excretion, does not elevate renin secretion by a direct renal action.

Animals↗
PubMed1980

Characterization of the beta-adrenergic receptor mediating secretion of parathyroid hormone.

In vitro incubation studies with bovine parathyroid gland slices compared the relative responsiveness of parathyroid hormone (PTH) secretion to isoprotherenol, epinephrine or norepinephrine. Isoproterenol was the most potent and norepinephrine the least potent of the three stimuli, suggesting a beta 2 type of an adrenergic response. However in this in vitro system, tazalol, a selective beta 1 adrenergic agonist significantly stimulated PTH secretion, whereas terbutaline, a selective beta 2 agonist had no effect. In addition, practolol, a selective beta 1 adrenergic antagonist blocked isoproterenol- or tazolol-stimulated PTH secretion. In vivo studies in normal human subjects showed that injection of te nonselective beta agonist, isoproterenol, (0.15 mg s.c.) significantly increased, whereas injection of the selective beta 2 agonist, terbulatine (0.3 mg s.c.) had no effect on serum PTH levels. These latter studies with putative selective beta adrenergic agents suggest that the beta adrenergic receptor mediating PTH secretion is of the beta 1 type (in contrast to the studies above with nonselective agents). The studies suggest that the beta adrenergic receptor mediating PTH secretion apparently differs from the classical beta 1 receptor described in th myocardium or the classical beta 2 receptor described in the bronchial smooth muscle.

Adrenergic beta-Agonists↗