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PubMed1995

Several anesthetics, but not diethyl ether, cause marked elevation of serum parathyroid hormone concentration in rats.

The effects of anesthetics on serum parathyroid hormone (PTH) concentrations were determined by a new homologous two-site immunoradiometric assay for rat PTH. Serum PTH concentrations (mean +/- SE) from ether-anesthetized rats (14.7 +/- 1.5 pg/ml, n = 22) were not significantly different from those of decapitated unanesthetized female rats (13.0 +/- 1.8 pg/ml, n = 21). Serum PTH concentrations in pg/ml (n = 4-14) for other anesthetics tested were: ketamine, 12.5 +/- 1.1; Na pentobarbital, 23.3 +/- 2.4; methoxyflurane (inhalation), 42.2 +/- 6.8; and xylazine combined with ketamine, 51.4 +/- 11.3 pg/ml. The latter two concentrations were significantly (p < 0.001) higher than the values for all other anesthetics and decapitation. Elevation of serum PTH induced by pentobarbital or ketamine + xylazine increased with time under anesthesia. Neither serum Ca2+ concentrations nor pH differed among any of the groups. We conclude that anesthesia induced by pentobarbital, methoxyflurane, or ketamine + xylazine in rats leads to a marked elevation of serum PTH levels that appears to be related to the duration of anesthesia and not due to any measurable fall in serum Ca2+.

Anesthetics↗
PubMed1980

Development of homologous immunological assays for human parathyroid hormone.

Antisera to a trichloroacetic-acid precipitate of human parathyroid hormone (PTH) were produced in goats. Two of these antisera (G36 and G31) were of high affinity, and the bovine and porcine hormones were less reactive. Synthetic peptides containing the amino-terminal region of human PTH reacted with both antisera; the 1--34 peptide (PTH-(1--34)), with the sequence proposed by Niall, Sauer, Jacobs, Keutmann, Segre, O'Riordan, Aurbach & Potts in 1974, was more reactive than that having the sequence proposed by Brewer, Fairwell, Ronan, Sizemore & Arnaud in 1972. The antisera were further characterized with a number of other native and synthetic fragments of human PTH and reacted poorly with fragments from the carboxy-terminal region of the molecule. Since the amino-terminal fragments did not account for all the immunoreactivity, it is assumed that the antisera had some recognition sites for the central part of the molecule. Highly purified human PTH-(1==84) was labelled with 125I and radioimmunoassays were developed using this tracer and antiserum G36. To avoid the problems associated with labelling human PTH with 125I, a labelled antibody assay was developed with G36 and an immunoadsorbent consisting of human PTH-(1--34) (sequence of Niall et al.) coupled to cellulose. A sensitive homologous amino-terminal specific assay was developed in this way.

Animals↗
PubMed1999

Bone resorption induced by parathyroid hormone is strikingly diminished in collagenase-resistant mutant mice.

Parathyroid hormone (PTH) stimulates bone resorption by acting directly on osteoblasts/stromal cells and then indirectly to increase differentiation and function of osteoclasts. PTH acting on osteoblasts/stromal cells increases collagenase gene transcription and synthesis. To assess the role of collagenase in the bone resorptive actions of PTH, we used mice homozygous (r/r) for a targeted mutation (r) in Col1a1 that are resistant to collagenase cleavage of type I collagen. Human PTH(1-34) was injected subcutaneously over the hemicalvariae in wild-type (+/+) or r/r mice four times daily for three days. Osteoclast numbers, the size of the bone marrow spaces and periosteal proliferation were increased in calvariae from PTH-treated +/+ mice, whereas in r/r mice, PTH-induced bone resorption responses were minimal. The r/r mice were not resistant to other skeletal effects of PTH because abundant interstitial collagenase mRNA was detected in the calvarial periosteum of PTH-treated, but not vehicle-treated, r/r and +/+ mice. Calcemic responses, 0.5-10 hours after intraperitoneal injection of PTH, were blunted in r/r mice versus +/+ mice. Thus, collagenase cleavage of type I collagen is necessary for PTH induction of osteoclastic bone resorption.

Animals↗
PubMed1987

Comparison of calcium effect on in vitro calcitonin and parathyroid hormone release by young and aged thyroparathyroid glands.

Serum immunoreactive parathyroid hormone (iPTH) and calcitonin (iCT) levels are higher in young than aged rats. However, serum calcium concentration does not change with age suggesting that the calcium regulation of PTH and CT secretion may be affected by aging. We compared iPTH and iCT secretion in vitro at low and high calcium concentrations using thyroparathyroid glands removed from young (2-3 months), adult (12-13 months), and old (24-27 months) F-344 male rats fed regular rat chow. Glands from each animal were incubated for 3 h in serum-free culture media containing 1.0 mM calcium and then transferred to media containing 2.5 mM calcium for another 3 h. Immunoreactive PTH and iCT concentrations of the media after each incubation period were determined by radioimmunoassay. Immunoreactive PTH and iCT secretion per pair of glands was significantly higher in glands from older animals regardless of calcium concentration. The decrease in iPTH, and increment in iCT, secretion in response to 2.5 mM calcium by glands from old rats was smaller than that observed for glands from young animals. These age-related changes in the regulation of secretion by calcium may contribute to the increased iPTH and iCT secretion and serum levels seen in older animals.

Aging↗
PubMed1988

Intracellular cascades in the parathyroid-hormone-dependent regulation of Na+/phosphate cotransport in OK cells.

Parathyroid hormone (PTH) increased intracellular cyclic AMP and reduces Na+/phosphate cotransport activity in OK cells [Malmström & Murer (1986) Am. J. Physiol. 251, C23-C31; Caverzasio, Rizzoli & Bonjour (1986) J. Biol. Chem. 261, 3233-3237]. It was also shown that PTH activates phosphoinositide metabolism in OK cells [Hruska, Moskowitz, Esprit, Civitelli, Westbrook & Huskey (1987) J. Clin. Invest. 79, 230-239]. In the present paper we show that tumour-promoting phorbol esters are effective in reducing Na+/phosphate cotransport. The Ca2+ ionophores A23187 and ionomycin had only a small effect on Na+/phosphate cotransport; added together, A23187 and phorbol esters showed a synergistic action. Phorbol esters and phorbol esters plus ionomycin stimulated prostaglandin synthesis as well as cyclic AMP production; acetylsalicylic acid prevented phorbol-ester-induced prostaglandin synthesis and cyclic AMP production, but had no effect on inhibition of Na+/phosphate cotransport. In suspensions of OK cells, PTH and thrombin produced a rise in intracellular Ca2+. In contrast with PTH, thrombin did not elevate cellular cyclic AMP in suspended OK cells. PTH and thrombin reduced Na+/phosphate cotransport in suspended OK cells. It is suggested that two regulatory cascades are involved in PTH action on Na+/phosphate cotransport: cyclic AMP/kinase A and Ca2+/diacylglycerol/kinase C.

Biological Transport↗
PubMed1982

Increase of whole-body calcium and skeletal mass in normal and osteoporotic adult rats treated with parathyroid hormone.

1. The effect of long-term administration of parathyroid hormone (PTH) on whole-body calcium and ash weight of individual bones has been studied in normal and osteoporotic adult female rats in order to examine whether such a treatment could induce a positive calcium balance. 2. Osteoporosis was induced by calcium restriction during pregnancy and lactation. Sequential measurements of whole-body calcium were made by neutron activation. 3. In non-osteoporotic intact and thyroparathyroidectomized rats a daily dose of 75 units of human PTH 1-34 given subcutaneously for 3 weeks increased whole-body calcium. 4. In osteoporotic animals 25-50 units of either bovine PTH 1-84 or human PTH 1-34 given subcutaneously twice daily for 6 weeks increased both whole-body calcium and ash weight of individual bones. Microradiographic examination of the tibiae indicates, however, that PTH administration does not result in the restoration of individual trabeculae lost during the development of osteoporosis. 5. The results show that PTH can enhance skeletal mass in both normal and osteoporotic rats. In osteoporotic animals the restoration of whole-body calcium and ash weight of individual bones is not accompanied by a return of the morphological structure of the tibia to normal.

Animals↗
PubMed2006

Intermittent parathyroid hormone therapy to increase bone formation.

Clinical data suggested that parathyroid hormone (PTH) might be effective in improving bone mass in patients with osteoporosis, providing its resorptive effects, which are particularly marked at cortical sites, were kept under control. We reviewed the evidence that intermittent PTH therapy is a valid treatment option whose predominant effect is bone anabolism. In cell culture studies, PTH affected both bone formation and bone resorption, suggesting that the net result of PTH therapy may be either bone gain or bone loss depending on the dosage, mode of administration, bone site, and animal species. Histological studies established that intermittent PTH therapy was associated with an increase in trabecular bone and, importantly, with improvements in trabecular and cortical microarchitectural parameters that have not been reported with antiresorptive drugs. This anabolic effect of intermittent PTH therapy translates into increased biomechanical strength, despite the increase in endocortical porosity seen in humans and nonhuman primates. The biochemical response profile to intermittent PTH therapy in clinical trials indicated a phase of isolated anabolism followed by an overall increase in bone remodeling that predominantly affected bone formation, the result being a large increase in spinal bone mineral density as early as the first treatment year. Thus, intermittent PTH therapy exerts predominantly anabolic effects on bone.

Animals↗
PubMed1987

Plasma parathyroid hormone during the development of spontaneous hypertension in rats.

Plasma parathyroid hormone levels (pPTH) have been measured by radioimmunoassay (RIA) in young spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto controls (WKY) aged from 6 to 16 weeks to assess the possible role of PTH during the development of hypertension. Three antisera were used in the RIAs. One antiserum was directed toward the inactive C-terminal fragment of PTH, another toward the bioactive N-terminal fragment (PTH 1-34), and a third was obtained by immunization against intact PTH 1-84. Blood pressures were measured by tail-cuff plethysmography with prewarming. Blood ionized calcium and sodium concentrations (b[Ca2+] and b[Na+]) were determined by ion-selective electrolyte analysis. No significant differences were observed between pPTH in the SHR compared with WKY during the development of hypertension. Neither were significant differences in b[Ca2+] or b[Na+] present at any age. The expected progression of hypertension in SHRs was observed and blood pressure was significantly greater in SHR than in WKY at all times. The results suggest that differences in pPTH and b[Ca2+] in SHR reported in other studies may be secondary phenomena to the establishment of hypertension. Our data suggest that PTH is not involved in the pathogenetic processes occurring during the development of spontaneous hypertension in rats.

Aging↗
PubMed1994

Cytochrome c oxidase activity in osteoclasts appeared in an early stage of parathyroid hormone treatment.

Osteoclasts which appeared in an early stage of parathyroid hormone (PTH) administration were examined using cytochrome c oxidase activity. In the period of 1-2 hr after intraperitoneal administration of PTH, two types of osteoclasts were observed. The first type had a well-developed ruffled border characterized by deeply infolded extracellular channels, and many endocytic vacuoles were observed, as seen in control osteoclasts. Many of the mitochondria contained in the first type were with the reaction products of the enzyme on the crystal membrane and within the intermembrane space (type 1 mitochondria), and the distribution of type 1 mitochondria was similar to that seen in control osteoclasts. The second type had a ruffled border characterized by unclear extracellular channels and cytoplasmic projections. The numerical percentage of type 1 mitochondria in the second type of osteoclasts (45.3%) was significantly smaller than that in the first type (79.9%). Mitochondria which had the reaction products of the enzyme only on the crystal membrane including those with no reaction product (type 2 mitochondria) were predominant in the second type of osteoclasts. These results include two possible ways in which a morphologically regressive change of the ruffled border can occur in osteoclasts during an early stage of PTH treatment, and cytochrome c oxidase activity is closely associated with the change in the ruffled border.

Animals↗
PubMed1974

Direct inhibitory effect of hypercalcemia on renal actions of parathyroid hormone.

The effects of calcium on the renal actions of parathyroid hormone (PTH) were studied in vivo and in vitro. In parathyroidectomized rats, variable levels of blood calcium concentration were induced by intravenous infusion of calcium. The renal responses to the injected PTH, i.e. phosphate and cyclic AMP excretion, were compared in these animals. After PTH injection, the increases of both phosphate and cyclic AMP excretion were less in the calcium-infused animals than in the control group without calcium infusion. There was an inverse correlation between the renal responses to PTH and plasma calcium concentration of 4.2-13.5 mg/100 ml. But calcium had no effect on phosphate excretion induced by infusion of dibutyryl cyclic AMP. In the in vitro experiments, the increase of cyclic AMP concentration in response to PTH was less in renal cortical slices taken from the calcium-infused animals than in ones from the control group without calcium infusion. Calcium also inhibited the activation of renal cortical adenylate cyclase in response to PTH, but calcium had no effect on phosphodiesterase. The data indicate that calcium directly inhibits renal actions of PTH both in vivo and in vitro. Such inhibitory mechanism is probably at or before the step of PTH-dependent cyclic AMP generation in the kidney.

Adenylyl Cyclase Inhibitors↗
PubMed1977

Response of phosphate transport to parathyroid hormone in segments of rabbit nephron.

The effects of bovine parathyroid hormone (PTH) on phosphate transport were examined in proximal convoluted tubules, proximal straight tubules, and cortical collecting ducts isolated from the rabbit kidney. The lumen-to-bath flux of phosphate (JlbPO4) and the bath-to-lumen flux (JblPO4) were measured simultaneously with [33P]phosphate and [32P]phosphate. In the proximal convoluted segments perfused with an ultrafiltrate of normal serum, PTH reduced the fluid absorption rate from 1.21 +/- 0.10 to 0.60 nl/mm-min but did not affect JlbPO4, which averaged 5.45 +/- 0.97 pmol/mm-min, or JblPO4, which was 0.50 +/- 0.08 pmol/mm-min. During perfusion with low bicarbonate-high chloride fluids at pH 7.4, the PTH-induced changes in fluid absorption were eliminated but no change occurred in phosphate transport. On the other hand in proximal straight segments JlbP04 was lower at 2.64 +/- 0.41 pmol/mm-min and was directly inhibited by PTH to 1.90 +/- 0.34 pmol/mm-min (P less than 0.001). Net phosphate transport was not observed in cortical collecting ducts in the presence or absence of PTH. These data suggest that phosphate absorption in the proximal tubule involves more than one transport system, that the effects of PTH on fluid absorption are not interdependent with the effects on phosphate transport, and that the proximal straight tubule appears to be an important site of PTH-sensitive phosphate transport.

Animals↗
PubMed2003

Parathyroid hormone induces the nuclear orphan receptor NOR-1 in osteoblasts.

Parathyroid hormone (PTH) significantly affects osteoblast function by altering gene expression. We have identified neuron-derived orphan receptor-1 (NOR-1) as a PTH-induced primary gene in osteoblastic cells. NOR-1, Nurr1, and Nur77 comprise the NGFI-B nuclear orphan receptor family and Nurr1 and Nur77 are PTH-induced primary osteoblastic genes. Ten nM PTH maximally induced NOR-1 mRNA at 2h in primary mouse osteoblasts and at 1h in mouse calvariae. Cycloheximide pretreatment did not inhibit PTH-induced NOR-1 mRNA. PTH activates cAMP-protein kinase A (PKA), protein kinase C (PKC), and calcium signaling. Forskolin (PKA activator) and PMA (PKC activator) mimicked PTH-induced NOR-1 mRNA. Ionomycin (calcium ionophore) and PTH(3-34), which do not activate PKA, failed to induce NOR-1 mRNA. PKA inhibition with H89 blocked PTH- and FSK-induced NOR-1 mRNA. PMA pretreatment to deplete PKC inhibited PMA-induced, but not PTH-induced, NOR-1 mRNA. We conclude that NOR-1 is a PTH-regulated primary osteoblastic gene that is induced mainly through cAMP-PKA signaling.

3T3 Cells↗
PubMed1990

Parathyroid hormone action on phosphate transport is inhibited by high osmolality.

Parathyroid hormone (PTH) produces rapid inhibition of Na(+)-phosphate cotransport, characterized by a decreased maximal rate of transport, and the inhibition is independent of de novo protein synthesis. The present study determined whether the action of PTH on Na(+)-phosphate cotransport is mediated, at least in part, by rapid endocytic internalization of Na(+)-phosphate cotransporters present in the plasma membrane. Horseradish peroxidase, a fluid-phase marker, was used to demonstrate the presence of endocytosis in opossum kidney (OK) epithelial cells in monolayer culture. An increase in medium osmolality to 500 mosmol/kgH2O, by addition of sucrose, produced 80% inhibition of endocytosis within 1 h. The inhibition was reversed on returning the cells to normal medium. Incubation of OK cell monolayers with PTH (10(-8) M) for 3 h at normal osmolality (281 mosmol/kgH2O) inhibited Na(+)-phosphate cotransport (4 min uptakes) by 56-67%. In hyperosmolar medium (513 mosmol/kgH2O), when endocytosis was inhibited, PTH inhibited Na(+)-phosphate cotransport by only 25-39%, a change that was significantly different from the inhibition in normal medium. Hyperosomolality had no effect on PTH inhibition of Na(+)-H+ exchange or on PTH stimulation of intracellular adenosine 3',5'-cyclic monophosphate. We conclude that the full inhibitory action of PTH on Na(+)-phosphate cotransport may require an intact endocytic mechanism.

Animals↗
PubMed1975

Influence of dialysate calcium concentration and vitamin D on serum parathyroid hormone during repetitive dialysis.

An acute rise or decrease in parathyroid hormone (PTH) secretion was found in 30 patients, dialyzed with, respectively, low (5 mg/100 ml) or high (7.5 mg/100 ml) calcium concentration. The percentage changes were, respectively, +35% and -47% when a N-terminal antiserum measuring predominantly the glandular PTH was used. Only relatively small changes, respectively, +3% and -17%, were found using a C-terminal antiserum which detects preferentially smaller PTH fragments. Predialysis serum PTH concentration increases significantly with increasing duration of repetitive hemodialysis treatment using an intermediate (6 and 6.4 mg/100 ml) concentration of calcium in the dialysate. No such increase could be found in two other groups of patients treated with high-calcium (7.5 mg/100 ml) dialysis. Moreover, a significant but temporary decrease in predialysis serum PTH concentration occurred two months after a rise in dialysate calcium concentration from 6 to 7.5 mg/100 ml. Treatment with pharmacologic doses of vitamin D3 in selected patients (renal osterdystrophy or children) always resulted in a definite suppression of serum PTH concentration during 14 treatment periods in ten patients. After cessation of vitamin D3 treatment, serum PTH concentration returned to high levels in four out of five patients. These data fail to confirm the long-term involution of secondary hyperparathyroidism using high-calcium dialysis. Vitamin D treatment, however, results in a much more pronounced decrease in serum PTH concentrations, but sustained therapy is necessary.

Adolescent↗
PubMed1994

Further definition of the protein kinase C activation domain of the parathyroid hormone.

The protein kinase C (PKC) activation domain of the parathyroid hormone (PTH) was believed to be the 28-34 region of the molecule. We have now shown that PTH-(29-32) is the smallest PTH fragment that can stimulate significantly membrane-associated PKC activity in ROS 17/2 rat osteosarcoma cells. As was previously shown for full-length PTH-(1-84) and the fully bioactive PTH-(1-34) fragment, there were two peaks in the PKC response to PTH-(29-32): one peak was obtained with low picomolar concentrations and the other with much higher nanomolar concentrations of the fragment. The PKC-activating ability was unaffected by the loss of Asn33 and Phe34, but it was abolished by removing His32. Thus, the PTH-(28-31) and PTH-(29-31) fragments did not stimulate membrane-associated PKC activity. The much larger PTH-(1-31) fragment also did not stimulate membrane-associated PKC activity, although it stimulated adenylyl cyclase as strongly as PTH-(1-34). This functional sensitivity to the loss of the polar His32 was not caused by a specific need for His or another polar amino acid in this position because replacing it with the apolar Leu did not abolish adenylyl cyclase or PKC activation. It is concluded that the minimum, fully functional PKC activation domain of the PTH molecule is Gln29-Asp30-Val31-His32.

Adenylyl Cyclases↗
PubMed2006

Perioperative parathyroid hormone levels in thyroid surgery.

OBJECTIVE: Perioperative hypocalcemia from temporary parathyroid gland dysfunction is common after thyroid surgery. No reliable cutoff values for parathyroid hormone (PTH) and the subsequent possibility of developing hypocalcemia exist. The purpose of this study is to determine a criterion for predicting hypocalcemia based on different PTH levels as cutoff values. STUDY DESIGN: Retrospective chart review. METHODS: A centralized database of intraoperative PTH levels was analyzed. PTH values approximately 10 minutes after excision of the thyroid gland and in the recovery room were obtained; serial ionized calcium levels were also analyzed. PTH values were then compared using chi-square analysis with significance defined as P < .05. A receiver operator characteristic (ROC) curve was also constructed to define sensitivities and specificities of different PTH levels as potential cutoff values. RESULTS: Eighty patients were identified meeting the study criteria between January 1999 and February 2005. Fourteen of the 80 (17.5%) patients became hypocalcemic during the hospital stay; none experienced permanent hypocalcemia. Patients who became hypocalcemic during their hospitalization were more likely to have a PTH level below 15 pg/mL (P < .01). Patients with a PTH level less than 15 pg/mL were more likely to develop hypocalcemia (P < .01). Finally, an ROC curve was constructed, allowing the surgeon to determine acceptable sensitivities and specificities and various PTH cutoff values. CONCLUSION: Low perioperative PTH levels significantly correlate with the presence of postoperative hypocalcemia but cannot be used to predict it. Using the ROC curve allows different chosen cutoff values to predict hypocalcemia with varying sensitivity and specificity.

Biomarkers↗
PubMed1998

The role of parathyroid hormone in the pathogenesis, prevention and treatment of postmenopausal osteoporosis.

Parathyroid hormone (PTH) is the principal regulator of bone remodeling in the adult skeleton. The acute in vivo effect of PTH is to increase bone resorption, although sustained increases in its circulating levels accelerate both formation and resorption. These divergent effects have focused attention on PTH as a factor contributing to bone loss in some postmenopausal women, as well as interest in its role as therapy for the disease. Sustained increases in PTH are classically seen in primary hyperparathyroidism. While still controversial, increasing evidence suggests that primary hyperparathyroidism is associated with increased rates of bone loss, particularly from cortical sites in the skeleton. It is clear that the remodeling space is increased in primary hyperparathyroidism, and that surgical correction of the disease leads to substantial increases in bone mass in patients with osteoporosis. Recently, secondary hyperparathyroidism has emerged as an important contributor to increased rates of bone turnover and bone loss in postmenopausal women. The etiology of secondary hyperparathyroidism in postmenopausal women is complex, and is probably related to alterations in vitamin D metabolism and tissue responsiveness to 1,25(OH)2vitamin D. PTH has emerged at the forefront of anabolic therapies for the treatment of postmenopausal osteoporosis. When given as a single agent, intermittent daily subcutaneous administration of PTH induces consistent gains in trabecular bone mass with more varying effects on the cortical envelope. However, recent therapeutic trials employing a second agent, most notably estrogen, give hope that this approach may provide the first truly efficacious anabolic therapy for this devastating disease.

Aged↗
PubMed1991

Role of parathyroid hormone in rat remnant kidney ammonium metabolism.

The role of parathyroid hormone (PTH) in ammonium metabolism in the rat remnant kidney was studied by examining the effects of parathyroidectomy (PTx) in rats with intact kidneys and with 5/6 nephrectomy (Nx). PTx in rats with intact kidneys caused a rise in urine pH and a decrease in urinary ammonium excretion without affecting in vitro ammonium production rate or the ammonium content in the cortex. Unexpectedly, the ammonium content in the medulla was markedly reduced by PTx so that the corticomedullary ammonium gradient was inverted. As compared to control rats, rats with 5/6 Nx had a lower urinary ammonium excretion rate, a higher in vitro ammonium production rate, and an increase in ammonium content in both cortex and medulla with reduced corticomedullary ammonium gradient. PTx in rats with 5/6 Nx led to a further decrease in urinary ammonium excretion, attenuated the increase in the in vitro ammonium production rate, and lowered the ammonium content in both cortex and medulla with inverted corticomedullary ammonium gradient. These effects of PTx in Nx rats were corrected by continuous PTH infusion with Alzet minipump. In summary, results from these studies indicate that PTH plays an important role in maintaining the urinary ammonium excretion. In rats with intact kidneys, PTH contributes to urinary ammonium excretion by increasing urinary acidification and medullary ammonium accumulation. In rats with reduced nephron mass, PTH enhances urinary ammonium excretion by stimulating ammonium production and retaining medullary ammonium in the remnant kidney.

Ammonia↗