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PubMed1990

The effect of parathyroid hormone on the acutely ischemic myocardium.

UNLABELLED: Parathyroid hormone (PTH) is reported to be a potent vasodilator. To determine if this action is beneficial in acute myocardial infarction (AMI) and is due to changes in prostacyclin or thomboxane, thirty dogs were anesthetized and instrumented (left atrial, coronary sinus, left main coronary, pulmonary artery and femoral artery catheters). AMI was induced by ligating the left anterior descending coronary artery. Either pentobarbital or alpha chloralose anesthesia was randomly assigned. Following LAD ligation, animals were randomized to receive PTH 0.008 nm/kg over 10 minutes every 30 minutes during the ischemic period or an equal volume of saline. Cardiac index, regional myocardial blood flow, O2 consumption and lactate production were measured. Infarct size was determined by computerized planimetry. PTH bioactivity was verified by adenyalate cyclase stimulating activity in rat osteosarcoma cells. Myocardial blood flow ranged from 81.5 to 155.2 ml/min/kg for normal myocardium. Cardiac index, O2 consumption, lactate production and myocardial perfusion was unaltered by the PTH administration. PTH reduced infarct size in dogs receiving pentobarbital but was deleterious in those receiving alpha chloralose. There was no difference in prostacyclin and thromboxane levels among groups. CONCLUSION: PTH is not beneficial in acute myocardial infarction.

Anesthetics↗
PubMed1986

Production of biologically active fragments of parathyroid hormone by isolated Kupffer cells.

Cleavage of parathyroid hormone (PTH) by isolated Kupffer cells from rat liver was examined. Iodinated PTH labeled at position 43 was converted into two radioactive fragments which were shown by Edman degradation to have residues 35 and 38 as their NH2 termini. Cleavage at these positions is characteristic of cathepsin D. Amino-terminal fragments were detected by bioassay of fractions obtained by high performance liquid chromatography. These fragments eluted in positions characteristic of the 1-34 and 1-37 peptides also previously shown to be produced by purified cathepsin D. The putative 1-37 fragment was rapidly converted to 1-34 upon digestion with cathepsin D, whereas the putative 1-34 fragment was not further digested by this enzyme, behavior previously shown to be characteristic of 1-37 and 1-34 bovine PTH. Fragmentation of PTH as measured by generation of fragments soluble in trichloroacetic acid was inhibited by methylamine, monensin, and ammonium chloride. In addition, monensin significantly inhibited production of both carboxyl- and amino-terminal fragments. Finally, active PTH fragments were also produced by elicited peritoneal macrophages. It is concluded that Kupffer cells, and other macrophages, can produce active fragments of PTH which appear in the medium. These fragments may be generated by cathepsin D within the cells.

Adenylyl Cyclases↗
PubMed1997

Induction of cyclooxygenase-2 by parathyroid hormone in human osteoblasts in culture.

OBJECTIVE: Parathyroid hormone (PTH) induced bone resorption by osteoclasts depends on the presence of osteoblasts. PTH induced production of prostaglandins by osteoblasts and induction of bone resorption by prostaglandins suggest that these autacoids may be implicated in the effects of PTH on bone. Our objective was to determine if the increase in prostaglandin production induced in human osteoblasts by PTH is due to an increase in cyclooxygenase-2 (COX-2) expression. METHODS: Primary cultures of human osteoblasts were obtained from specimens of trabecular bone. Confluent cells were treated with PTH, dexamethasone or compound NS-398, a specific COX-2 inhibitor. The concentration of prostaglandin E2 (PGE2) in the supernatants was determined by radioimmunoassay and COX-2 mRNA levels evaluated by Northern blot. RESULTS: PTH induced COX-2 mRNA expression and PGE2 production. These effects were time and concentration dependent and were inhibited by dexamethasone. Compound NS-398 reduced PGE2 production to the same extent as dexamethasone, and neither compound had an additive effect on this variable. CONCLUSION: These results show that PTH induces COX-2 expression in human osteoblasts in culture and suggest that this isoenzyme is the main factor in the control of prostaglandin synthesis in these experimental conditions.

Cells, Cultured↗
PubMed1977

Nonautonomy of parathyroid hormone and urinary cyclic AMP in primary hyperparathyroidism.

This study demonstrates that appreciable changes in serum parathyroid hormone and urinary cyclic AMP occur during experimentally induced hyper- and hypocalcemia in almost all patients with primary hyperparathyroidism regardless of histology. A single patient with tertiary hyperparathyroidism also demonstrated a significant elevation of serum parathyroid hormone and urinary cyclic AMP in response to EDTA induced reduction in ionized calcium. Thus, total autonomy of hormone secretion was not present in the great majority of the patients with a parathyroid adenoma, parathyroid hyperplasia, or the single patient with tertiary hyperparathyroidism. Therefore, preoperative evaluation of the rsponse of urinary cyclic AMP and serum parapthyroid hormone to EDTA or calcium infusion will not distinguish parathyroid adenomas from hyperplasia on the basis of total autonomy of hormone secretion. If a difference in secretory control is present between parathyroid adenomas and parathyroid hyperplasia, it is more subtle than total autonomy for adenomas and nonautonomy for hyperplasia.

Adenoma↗
PubMed2004

Interaction of a farnesylated protein with renal type IIa Na/Pi co-transporter in response to parathyroid hormone and dietary phosphate.

Treatment with PTH (parathyroid hormone) or a high-P(i) diet causes internalization of the type IIa sodium-dependent phosphate (Na/P(i) IIa) co-transporter from the apical membrane and its degradation in the lysosome. A dibasic amino acid motif (KR) in the third intracellular loop of the co-transporter is essential for protein's PTH-induced retrieval. To elucidate the mechanism of internalization of Na/P(i) IIa, we identified the interacting protein for the endocytic motif by yeast two-hybrid screening. We found a strong interaction of the Na/P(i) IIa co-transporter with a small protein known as the PEX19 (human peroxisomal farnesylated protein; PxF, Pex19p). PEX19 can bind to the KR motif, but not to a mutant with this motif replaced with NI residues. PEX19 is highly expressed in mouse and rat kidney. Western blot analysis indicates that PEX19 is located in the cytosolic and brush-border membrane fractions (microvilli and the subapical component). Overexpression of PEX19 stimulated the endocytosis of the Na/P(i) IIa co-transporter in opossum kidney cells in the absence of PTH. In conclusion, the present study indicates that PEX19 may be actively involved in controlling the internalization and trafficking of the Na/P(i) IIa co-transporter.

Amino Acid Sequence↗
PubMed1987

Age-related rise in parathyroid hormone in man: the use of intact and midmolecule antisera to distinguish hormone secretion from retention.

Circulating levels of parathyroid hormone (PTH) rise with age in normal men and women. To resolve the basis for this observation we measured iPTH in 137 normal men and women, age 23 to 85 years, using two antisera which responded to different portions of the PTH molecule. A midmolecule assay (Mid-PTH) employed antiserum NG-5, which recognizes mid- and carboxy-terminal portions of hPTH, whereas antiserum CK-67, which recognizes determinants in the 1-34 hPTH sequence, was used to measure intact PTH (NH2-PTH). Two-hour fasting urine was collected for measurement of creatinine clearance and excretion indices of phosphorus and cyclic AMP. Serum was analyzed for 25-hydroxyvitamin D (25-OHD) in addition to iPTH. Mid-PTH rose significantly with age in the 72 women (r = 0.38, p less than 0.001) and in the 65 men (r = 0.40, p less than 0.001). NH2-PTH rose with age in women (r = 0.23, p less than 0.05), but a change in men was not significant (r = 0.19, n.s.). Cyclic AMP excretion rose significantly with age in both women (r = 0.42) and men (r = 0.41), whereas phosphorus excretion rose significantly in women only (r = 0.32, p less than 0.01). 25-OHD levels were 27.5 +/- 1.3 ng/ml for women and 26.1 +/- 1.2 ng/ml for men. No change in 25-OHD was observed with age in women, and a significant decrease in men was due entirely to extremely high values in three young subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Relaxation of rat gastrointestinal smooth muscle by parathyroid hormone.

In this study we investigated whether parathyroid hormone (PTH) can produce relaxation of gastrointestinal (GI) smooth muscle as it has been reported to do for vascular and uterine smooth muscle. Muscle tissue preparations from rat stomach, duodenum, ileum, or colon were mounted in a 37 degrees C tissue bath and perfused with oxygenated medium. Changes in isometric tension were recorded with a force-displacement transducer connected to a polygraph. Decreases in either resting tension or agonist-induced tension (0.5-1.0 microM acetylcholine or carbachol) were observed within 1-2 min of PTH addition and were reversible upon removal of the peptide. All GI regions tested were responsive to PTH. Synthetic rPTH-(1-34) (0.1-100 nM) produced a dose-dependent relaxation of both fundic (ED50 = 5.2 nM) and colonic (ED50 = 2.5 nM) muscle strips. At 100 nM, a 90% decrease in fundic tension and a 70% decrease in colonic tension were seen. At 100 nM, bPTH-(1-34), but not bPTH-(7-34) or rat calcitonin gene-related peptide, also was effective in relaxing fundic or colonic muscle. Similarly, in the fundic muscle, 500 nM bPTH-(3-34) alone was ineffective, but it inhibited the effect of 5 nM rPTH-(1-34) when both peptides were tested in combination. Likewise, 100 nM bPTH-(3-34) also inhibited the relaxation induced by 5, 10, or 100 nM bPTH-(1-34). The results show PTH to be highly effective in nanomolar concentrations in causing relaxation of GI smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Impaired osteoclast formation in bone marrow cultures of Fgf2 null mice in response to parathyroid hormone.

Fibroblast growth factor (FGF)-2 and parathyroid hormone (PTH) are potent inducers of osteoclast (OCL) formation, and PTH increases FGF-2 mRNA and protein expression in osteoblasts. To elucidate the role of endogenous FGF-2 in PTH responses, we examined PTH-induced OCL formation in bone marrow cultures from wild type and mice with a disruption of the Fgf2 gene. FGF-2-induced OCL formation was similar in marrow culture from both genotypes. In contrast, PTH-stimulated OCL formation in bone marrow cultures or co-cultures of osteoblast-spleen cells from Fgf2-/mice was significantly impaired. PTH increased RANKL mRNA expression in osteoblasts cultures from both genotypes. After 6 days of treatment, osteoprotegerin protein in cell supernatants was 40-fold higher in vehicle-treated and 30-fold higher in PTH-treated co-cultures of osteoblast and spleen cells from Fgf2-/mice compared with Fgf2+/+ mice. However, a neutralizing antibody to osteoprotegerin did not rescue reduced OCL formation in response to PTH. Injection of PTH caused hypercalcemia in Fgf2+/+ but not Fgf2-/mice. We conclude that PTH stimulates OCL formation and bone resorption in mice in part by endogenous FGF-2 synthesis by osteoblasts. Because RANKL- and interleukin-11-induced OCL formation was also reduced in bone marrow cultures from Fgf2-/mice, we further conclude that endogenous FGF-2 is necessary for maximal OCL formation by multiple bone resorbing factors.

Acid Phosphatase↗
PubMed2004

Response of induced bone defects in horses to collagen matrix containing the human parathyroid hormone gene.

OBJECTIVE: To determine whether human parathyroid hormone (hPTH) gene in collagen matrix could safely promote bone formation in diaphyseal or subchondral bones of horses. ANIMALS: 8 clinically normal adult horses. PROCEDURE: Amount, rate, and quality of bone healing for 13 weeks were determined by use of radiography, quantitative computed tomography, and histomorphometric analysis. Diaphyseal cortex and subchondral bone defects of metacarpi were filled with hPTH(1-34) gene-activated matrix (GAM) or remained untreated. Joints were assessed on the basis of circumference, synovial fluid analysis, pain on flexion, lameness, and gross and histologic examination. RESULTS: Bone volume index was greater for cortical defects treated with hPTH(1-34) GAM, compared with untreated defects. Bone production in cortical defects treated with hPTH(1-34) GAM positively correlated with native bone formation in untreated defects. In contrast, less bone was detected in hPTH(1-34) GAM-treated subchondral bone defects, compared with untreated defects, and histology confirmed poorer healing and residual collagen sponge. CONCLUSIONS AND CLINICAL RELEVANCE: Use of hPTH(1-34) GAM induced greater total bone, specifically periosteal bone, after 13 weeks of healing in cortical defects of horses. The hPTH(1-34) GAM impeded healing of subchondral bone but was biocompatible with joint tissues. Promotion of periosteal bone formation may be beneficial for healing of cortical fractures in horses, but the delay in onset of bone formation may negate benefits. The hPTH(1-34) GAM used in this study should not be placed in articular subchondral bone defects, but contact with articular surfaces is unlikely to cause short-term adverse effects.

Analysis of Variance↗
PubMedDate not supplied

Nucleotide sequence of bovine parathyroid hormone messenger RNA.

The sequence of bovine parathyroid hormone mRNA has been determined by sequence analysis of near full-length cloned DNA complementary to the mRNA. Restriction fragments hybridized to the mRNA and extended toward the 5' terminus with reverse transcriptase were analyzed to derive the sequence not present in cDNA. The reverse transcripts were heterogeneous in length with three major stopping points within 8 nucleotides of each other and a minor stop about 30 bases further toward the 5' terminus of the mRNA. The sequence of the gene corresponding to the minor reverse transcript begins with the sequence 5' XXXATATATAAAA which contains the consensus sequence for a TATA box, a putative eukaryotic promoter sequence. Assuming that the major reverse transcriptase stop nearest the 5' terminus of the mRNA, which is 24 bases downstream from the TATA box, represents the beginning of bovine PTH mRNA, the mRNA contains 672 nucleotides, 100 in the 5' noncoding region, 348 in the coding region and 224 in the 3' noncoding region. Bovine PTH mRNA contains 38% G and C bases. The 3' noncoding region is particularly rich in A and U bases with the last 100 nucleotides of the molecules containing 46% U and 32% A. As with other mRNAs, the sequences CG and UAG occur much less than expected. The 5' noncoding region does not contain an AUG before the initiator codon and contains two potential regions that could base-pair with sequences near the 3' terminus of 18S ribosomal RNA. The sequence AAUAAA is present 14 nucleotides from the polyadenylic acid at the 3' terminus. Bovine PTH mRNA exhibits extensive homology with human PTH mRNA.

Animals↗
PubMed2000

Stimulation of extracellular signal-regulated kinases and proliferation in rat osteoblastic cells by parathyroid hormone is protein kinase C-dependent.

Parathyroid hormone (PTH) is known to have both catabolic and anabolic effects on bone. The dual functionality of PTH may stem from its ability to activate two signal transduction mechanisms: adenylate cyclase and phospholipase C. Here, we demonstrate that continuous treatment of UMR 106-01 and primary osteoblasts with PTH peptides, which selectively activate protein kinase C, results in significant increases in DNA synthesis. Given that ERKs are involved in cellular proliferation, we examined the regulation of ERKs in UMR 106-01 and primary rat osteoblasts following PTH treatment. We demonstrate that treatment of osteoblastic cells with very low concentrations of PTH (10(-12) to 10(-11) m) is sufficient for substantial increases in ERK activity. Treatment with PTH-(1-34) (10(-8) m), PTH-(1-31), or 8-bromo-cAMP failed to stimulate ERKs, whereas treatment with phorbol 12-myristate 13-acetate, serum, or PTH peptides lacking the N-terminal amino acids stimulated activity. Furthermore, the activation of ERKs was prevented by pretreatment of osteoblastic cells with inhibitors of protein kinase C (GF 109203X) and MEK (PD 98059). Treatment of UMR cells with epidermal growth factor (EGF), but not PTH, promoted tyrosine phosphorylation of the EGF receptor. Transient transfection of UMR cells with p21(N17Ras) did not block activation of ERKs following treatment with low concentrations of PTH. Thus, activation of ERKs and proliferation by PTH is protein kinase C-dependent, but stimulation occurs independently of the EGF receptor and Ras activation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1987

Parathyroid hormone in sodium-dependent hypertension.

Plasma parathyroid hormone (pPTH) levels have been assessed in three separate radioimmunoassay systems in samples from Wistar-Kyoto rats. The animals were subjected to one of three dietary regimens throughout the study period: Group 1 animals consumed normal rat chow and drank tap water; Group 2 animals consumed normal rat chow and tap water was replaced with 0.5% saline solution; Group 3 animals consumed normal rat chow to which 2.5% CaCO3 (by weight) had been added and also drank 0.5% saline solution. Animals had consumed these diets for approximately 7 months prior to sacrifice for blood collection. Blood pressure was measured by tail cuff plethysmography in these animals and, as previously reported, saline consuming animals showed a moderate hypertension (Gp 2) only when diets did not contain added calcium (Gp 3). In the week prior to sacrifice, mean blood pressures were: Gp 1: 128.0 +/- 3.46 mmHg; Gp 2: 140.2 +/- 3.15 mmHg; and Gp 3: 133.5 +/- 2.90 mmHg. Three assay systems were used to measure pPTH levels from trunk blood samples obtained by guillotine decapitation. One assay used an antiserum directed toward the vasoactive N terminal fragment 1-34 and produced pPTH measurements of 0.74 +/- 0.05 ng/ml in Gp 1 animals, 1.04 +/- 0.07 ng/ml in Gp 2 animals and 1.12 +/- 0.08 ng/ml in Gp 3 animals. This pattern was consistent with that obtained by another antiserum which had been raised against the intact 1-84 PTH molecule and produced values of 0.25 +/- 0.03 ng/ml in Gp 1 animals, 0.55 +/- 0.07 ng/ml in Gp 2 animals and 0.74 +/- 0.04 ng/ml in Gp 3 animals. Antiserum raised against the C-terminal did not show any difference in pPTH across groups. We conclude that saline consumption may increase some portions of circulating PTH. Such elevation of pPTH may not be a pathophysiological component in the sodium dependent elevation of blood pressure since animals concurrently consuming both saline and calcium supplemented diets retained elevated pPTH levels even though blood pressures did not differ from controls. Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption.

Animals↗
PubMed1989

[Clinical studies using a highly sensitive radioimmunoassay for mid-region and carboxy terminus of parathyroid hormone in normal, hypo- and hypercalcemic states].

Parathyroid hormone radioimmunoassay (RIA), specific for mid-region of the PTH molecule, has been proven to be extremely useful for the differential diagnosis of abnormal calcium metabolism. Recently, we developed a highly sensitive RIA for PTH, consisting of PTH antiserum (CH9), 125I labelled Tyr42 hPTH (43-68) and synthetic hPTH (1-84) as standard. This RIA cross-reacted with mid-region and carboxyl terminals of PTH. The within-assay and between-assay coefficients of variation were less than 4.6% and less than 8.6%, respectively. The limit of detection was 50pg/ml. The levels of serum calcium, serum phosphate, serum creatinine, Tmpo4/GFR and creatinine clearance (Ccr) in normal healthy volunteers aged 20 to 50 years remained almost constant and showed 9.24 +/- 0.34mg/dl (mean +/- SD, n = 242), 3.34 +/- 0.38mg/dl (n = 242), 0.870 +/- 0.121mg/dl (n = 242), 3.20 +/- 0.54mg/dl GF (n = 189) and 103 +/- 17ml/min (n = 137), respectively. All healthy volunteers (n = 326) had measurements of PTH in the blood. From 20 to 50 years, normal PTH mean was 374 +/- 97pg/ml (+/- SD, n = 237) and ranged from 180-568pg/ml, and from 60 to 80 years it was 471 +/- 133pg/ml (n = 34) and ranged from 205-737pg/ml. Since we found that PTH was markedly elevated above normal when Ccr was below 40ml/min, and PTH was very significantly correlated with the reciprocal of Ccr (r = 0.8996, P less than 0.001) using a multivariate analysis, all of the patients whose Ccr was higher than 40ml/min were selected and examined in the following studies. Serum PTH values completely separated patients with surgically proven primary hyperparathyroidism (1 degree HPT) from malignant associated hypercalcemia (MAH), and patients with idiopathic hypoparathyroidism (IHP) from pseudohypoparathyroidism (PHP), both of which were diagnosed by Ellsworth-Howard test. PTH values in all of the patients with 1 degree HPT (n = 23) were above normal, but those with MAH (n = 6) were below the normal or lower normal range. PTH values in patients with PHP (n = 7) showed above normal, while those with IHP (n = 5) were below the normal range. PTH was normalized in post operative status in all patients after parathyroidectomy (n = 6). These results indicate that this PTH RIA is extremely useful for the differential diagnosis in diseases with calcium abnormalities.

Adolescent↗
PubMed1998

Calcium intake by rats: influence of parathyroid hormone, calcitonin, and 1,25-dihydroxyvitamin D.

We examined the contribution of the primary hormones of calcium homeostasis to the control of calcium intake in the rat. Male Sprague-Dawley rats with 50 mM CaCl2 solution as their only source of calcium received subcutaneous hormone infusions for 13 days. Parathyroid hormone (PTH; 40, 80, or 160 ng/h) produced sustained dose-related decreases in CaCl2 intake. High doses of calcitonin (CT; 32 or 64 ng/h) increased CaCl2 intake transiently, and low doses (4, 8, or 16 ng/h) had no effect. 1,25-Dihydroxyvitamin D [1,25(OH)2D] in doses > 1 ng/h initially increased CaCl2 intake, but the effects of moderate doses (2 or 4 ng/h) tended to dissipate, and the sustained effect of high doses (8 or 16 ng/h) was to reduce CaCl2 intake. Infusions of combinations of the hormones had effects consistent with their individual actions: there was no evidence for synergy. Based on changes in plasma hormone concentrations, it appeared that most of the infusions had effects within the physiological range. Consistent with hypotheses that calcium appetite is mediated by circulating calcium, PTH and CT infusions produced reciprocal changes in plasma calcium concentrations and CaCl2 intake. However, the finding that 1,25(OH)2D elevated both plasma calcium concentrations and CaCl2 intake raises the possibility that one or more of the hormones may mediate calcium appetite directly.

Animals↗
PubMed2000

Adverse effects of an active fragment of parathyroid hormone on rat hippocampal organotypic cultures.

Adverse effects of an active fragment of parathyroid hormone (PTH(1 - 34)), a blood Ca(2+) level-regulating hormone, were examined using rat hippocampal slices in organotypic culture. Exposure of cultured slice preparations to 0.1 microM PTH(1 - 34) for 60 min resulted in a gradual increase in the intracellular Ca(2+) concentration ([Ca(2+)](i)); this effect was most obvious in the apical dendritic region of CA1 subfield. When PTH(1 - 34) at a lower concentration (1 nM) was added to the culture medium and its toxic effects examined using a propidium iodide intercalation method, significant toxicity was seen 3 days after exposure and increased with time. Cells in the CA1 region seemed more vulnerable to the hormone than cells in other regions. At 1 week of exposure, the toxic effects were dose-dependent over the range of 0.1 pM to 0.1 microM, the minimum effective dose being 10 pM. The adverse effects were not induced either by the inactive fragment, PTH(39 - 84), or by an active fragment of PTH-related peptide (PTHrP(1 - 34)), an intrinsic ligand of the brain PTH receptor. The PTH(1 - 34)-induced adverse effects were significantly inhibited by co-administration of 10 microM nifedipine, an L-type Ca(2+) channel blocker, but not by co-administration of blockers of the other types of Ca(2+) channel. The present study demonstrates that sustained high levels of PTH in the brain might cause degeneration of specific brain regions due to Ca(2+) overloading via activation of dihydropyridine-sensitive Ca(2+) channels, and suggests that PTH may be a risk factor for senile dementia. British Journal of Pharmacology (2000) 129, 21 - 28

Animals↗
PubMed1988

The effects of parathyroid hormone or 1,25-dihydroxyvitamin D3 on monocyte-osteoclast fusion.

3H-thymidine-labeled blood monocytes were cultured with osteoclasts in the presence or absence of parathyroid hormone or 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) in order to evaluate (1) the percentage of monocytes capable of fusing with osteoclasts, (2) if parathyroid hormone or 1,25(OH)2D3 influences the contribution of blood monocytes to osteoclast nuclear turnover. We found that within 24 hours of culture, about 8% of blood monocytes fuse with osteoclasts regardless of the presence of parathyroid hormone (PTH) or 1,25(OH)2D3. On the other hand, formation of non-osteoclastic giant cells by fusion of monocytes is enhanced by 5 x 10(-9) M 1,25(OH)2D3 but only in the presence of the bone resorptive cells.

Acid Phosphatase↗
PubMed1984

[Urinary phosphate and cyclic adenosine monophosphate response to intravenous administration of synthetic human parathyroid hormone-(1-34) in idiopathic hypoparathyroidism, pseudohypoparathyroidism, pseudopseudohypoparathyroidism and normal subjects].

The response to exogenous parathyroid hormone (PTH) with urinary excretion of phosphate and cyclic adenosine monophosphate (cAMP) was tested by the use of synthetic human parathyroid hormone (1-34) [hPTH-(1-34)] on 59 patients with hypocalcemia and normal or high serum inorganic phosphorus and normal renal function without a history of parathyroidectomy for differentiation between idiopathic hypoparathyroidism (IHP), pseudohypoparathyroidism (PHP) and related diseases along with 18 normal subjects. A positive phosphaturic response to exogenous PTH was defined as the increment of 2 hours phosphate excretion (delta P) of more than 35 mg. A positive urinary cAMP response to exogenous PTH was defined as the increment by more than 1 mumole per one hour (delta cAMP) and the increase of 1 hour excretion by more than 10 times. Increments of 2 hours urinary phosphate excretion in response to hPTH-(1-34) 100 units were 60.5 +/- 7.7 mg (mean +/- SEM) in 27 patients with IHP, 23.5 +/- 5.9 mg in 21 patients with PHP type I and 24.9 +/- 4.0 mg in 17 normal subjects. Increments of 1 hour urinary cAMP excretion in response to hPTH-(1-34) 100 units were 12.0 +/- 1.5 mumole in 27 patients with IHP, 0.33 +/- 0.10 mumole in patients with PHP type I and 23.6 +/- 5.8 mumole in 15 normal subjects. Ratios of 1 hour urinary cAMP excretion were 97 +/- 10 in 27 patients with IHP, 3.6 +/- 0.5 in 21 patients with PHP type I and 54 +/- 14 in 15 normal subjects. Positive phosphaturic and negative urinary cAMP response was encountered in 3 out of 21 patients with PHP type I in response to hPTH-(1-34). This exaggerated phosphaturic response should be considered as due to the influence of treatment with Ca or vitamin D derivatives.

Adolescent↗
PubMed2003

Parathyroid hormone (PTH) secretion, PTH mRNA and calcium-sensing receptor mRNA expression in equine parathyroid cells, and effects of interleukin (IL)-1, IL-6, and tumor necrosis factor-alpha on equine parathyroid cell function.

Parathyroid hormone (PTH) is secreted by the chief cells of the parathyroid gland in response to changes in ionized calcium (Ca(2+)) concentrations. In this study, we measured PTH secretion, and PTH mRNA and calcium-sensing receptor (CaR) mRNA expression by equine parathyroid chief cells in vitro. We also evaluated the effects of interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha on PTH secretion, and PTH and CaR mRNA expression. The relationship between PTH and Ca(2+) was inversely related. PTH secretion decreased from 100% (day 0) to 13% (day 30). PTH mRNA expression declined from 100% (day 0) to 25% (day 30). CaR mRNA decreased from 100% (day 0) to 16% (day 30). Chief cells exposed to high (2.0 mM) Ca(2+) concentrations had a lower PTH mRNA expression compared with low Ca(2+) concentrations. Ca(2+) concentrations had no effect on CaR mRNA expression. The inhibitory effect of high Ca(2+) concentrations on PTH secretion also declined over time. After day 10, there was no significant difference in PTH secretion between low and high Ca(2+ )concentrations. IL-1beta decreased both PTH secretion (75%) and PTH mRNA expression (73%), and resulted in a significant overexpression of CaR mRNA (up to 142%). The effects of IL-1beta were blocked by an IL-1 receptor antagonist. IL-1beta decreased the Ca(2+) set-point from 1.4 mM to 1.2 mM. IL-6 decreased PTH secretion (74%), but had no effect on PTH and CaR mRNA expression. TNF-alpha had no effect on PTH secretion, and PTH and CaR mRNA expression. In summary, the decreased responsiveness of parathyroid cells to Ca(2+) from 0 to 30 days can be explained, in part, by the reduced CaR expression. IL-1beta and IL-6 but not TNF-alpha affected parathyroid function in vitro and may be important in influencing PTH secretion in the septic horse.

Animals↗