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PubMed1999

Post-transcriptional regulation of the parathyroid hormone gene by calcium and phosphate.

Parathyroid hormone messenger RNA levels are regulated by calcium, phosphate and 1,25-dihydroxyvitamin D3. Dietary induced hypocalcaemia increases and hypophosphataemia decreases parathyroid hormone mRNA levels post-transcriptionally. This regulation is mediated by binding of parathyroid cytosolic proteins to the parathyroid hormone mRNA 3'-untranslated region, and in particular the terminal 60 nucleotides of the 3'-untranslated region, thereby determining RNA stability.

3' Untranslated Regions↗

PubMedDate not supplied

Laboratory comparison of diagnostic specificity of intact hormone and region-specific immunoassays of parathyroid hormone.

A 2-site immunochemiluminometric assay (ICMA) for intact parathyroid hormone (PTH) has been developed to overcome the problems of limited sensitivity and specificity associated with conventional PTH immunoassays. The present investigation assesses the relative merits of the 2-site intact PTH (ICMA) and a midmolecule PTH radioimmunoassay (RIA). Immunoassay profiles of dispersed hyperparathyroid cell supernatants and hyperparathyroid sera obtained during parathyroidectomy and from renal failure patients, fractionated by gel filtration chromatography, facilitated a direct comparison of the specificity of PTH immunoassays. Using gel filtration matrices which permitted the separation of intact hormone, large C-terminal fragment(s), and a small midmolecule fragment in adenomatous cell supernatant and peripheral sera, the intact PTH (ICMA) assay consistently yielded a single peak of immunoreactivity. In contrast, the midmolecule RIA yielded 2 and 3 broad peaks of immunoreactivity after fractionation of serum and adenomatous cell supernatant, respectively. There was no evidence for the secretion of a small midregion fragment in vitro or its peripheral derivation in vivo. These studies demonstrate the superior specificity of the 2-site intact PTH assay compared with a midmolecule RIA and, thus, confirm the potential diagnostic superiority of the ICMA.

Calcium↗

PubMed1986

Effect of synthetic bovine parathyroid hormone in dairy cows: prevention of hypocalcemic parturient paresis.

Intravenous infusion of synthetic bovine parathyroid hormone for 96 h increased 1,25-dihydroxyvitamin D, Mg, Ca, and hydroxyproline in plasma of pregnant cows within 16, 24, 48, and 72 h, respectively. Plasma Ca concentration was maximal at the end of the 96-h infusion (15.1 mg/100 ml). Plasma concentration of 1,25-dihydroxyvitamin D at 96 h was twice that before parathyroid hormone infusion, indicating that parathyroid hormone stimulated 1,25-dihydroxyvitamin D production in the presence of hypercalcemia. The urinary excretion of hydroxyproline indicated that at least 48 h of parathyroid hormone stimulation was required to stimulate bone resorption in the pregnant cow. Eight periparturient cows were on a high Ca diet prepartum. Four cows were treated with intravenous parathyroid hormone prior to parturition. Four cows were untreated. All four untreated cows developed parturient paresis. None of the cows treated with parathyroid hormone developed parturient paresis. However, two cows that received parathyroid hormone for less than 24 h prior to parturition became hypocalcemic, but not recumbent. Plasma Ca concentrations remained within normal limits in the two other cows that received greater than 60 h parathyroid hormone infusion prior to parturition. We conclude that exogenous parathyroid hormone (1-34) can prevent parturient paresis if administered at least 60 h prior to parturition.

Animals↗

PubMed2002

Parathyroid hormone for treatment of osteoporosis.

BACKGROUND: Osteoporosis is a common condition associated with multiple deleterious consequences. No therapy entirely abolishes fracture risk. METHODS: A MEDLINE database (1966 to the present) search was performed for randomized controlled trials in humans using the keywords osteoporosis and parathyroid hormone (PTH) or parathyroid hormone and fracture. The Cochrane database was searched using the search terms osteoporosis and parathyroid hormone. RESULTS: Parathyroid hormone (usually subcutaneous) dosages varied markedly across the 20 randomized controlled trial studies retrieved. In the range of 50 to 100 micro g/d, effects may be dose-related. Results of larger trials (up to 1637 patients) were conflicting as to whether effects were limited to the spine and suggested detrimental effects on radius bone mineral density. Little data analyzed the effects of PTH in older vs younger subjects or directly compared the effects by sex. Increases in spine bone mineral density are induced by PTH in postmenopausal osteoporosis, glucocorticoid-induced osteoporosis, and idiopathic osteoporosis. Parathyroid hormone may protect against gonadotropin-releasing hormone agonist-related bone loss. Effects are less clear at nonspine sites when PTH is used as part of combination or sequential therapies or for treatment of glucocorticoid-induced osteoporosis. Parathyroid hormone decreased the incidence of radiographically detected spinal fractures. The numbers of nonvertebral fractures were too low to be broken down by individual site. Parathyroid hormone injections were difficult for some patients to comply with. Occasionally, PTH-associated hypercalcemia may be dose-dependent, often manifesting early in treatment. An increase in cancer risk from PTH is not reported in humans. CONCLUSIONS: Parathyroid hormone decreases vertebral fractures and increases spinal bone density in postmenopausal osteoporosis and glucocorticoid-induced osteoporosis, but at the expense of a decrease in radius bone density. The long-term safety and nonvertebral fracture efficacy are unknown.

Adult↗

PubMed1975

A comparison of the effects of the calcitonins, steroid hormones and thyroid hormones on the response of bone to parathyroid hormone in tissue culture.

A bone culture system was used to compare the effects of several hormones on the response of 5-day-old mouse calvaria to parathyroid hormone (PTH). The results showed that salmon calcitonin was almost 10-5 times more active than any other hormone in preventing the PTH-induced release of calcium and caused a dose-related inhibition of calcium release over a range of 0-2-200 milli MRC units/culture. A high dose of calcitonin (200 milli MRC units) caused a net accretion of calcium in the absence of PTH. Progesterone and testosterone were more active than the naturally occurring oestrogens although a synthetic oestrogen (stillboestrol diphosphate) had approximately the same potency. High concentrations of these hormones caused a net accretion of calcium whether or not PTH was present. Cortisol was only effective at high doses, as was the steroid precursor cholesterol. In the present culture system the thyroid hormones (triiodothyronine and thyroxine) inhibited the action of PTH. It was concluded that these agents acted in a similar fashion to the oestrogens. That is, they prevented the accumulation of citric acid induced by PTH by reducing the rate of glycolysis. None of the hormones affected the inhibition of citrate oxidation caused by PTH. The results also showed that, whilst these hormones inhibited PTH-mediated bone resorption, they had an action on bone independent of PTH. Experiments with clomiphene citrate failed to demonstrate an oestrogen receptor in bone.

Animals↗

PubMed2001

Early effect of parathyroid hormone (1-34) on implant fixation.

Intermittent systemic administration of parathyroid hormone increases bone formation by stimulating osteoblastic activity. The current study determined how parathyroid hormone (1-34) administration influences the bony fixation of stainless steel screws with time. A screw was implanted in the left tibia and a metal rod was implanted in the right tibia in 30 adult male rats that then were injected three times a week with human parathyroid hormone (1-34) at 60 microg/kg/injection (n = 15) or saline (n = 15). The animals were euthanized after 1, 2, or 4 weeks of treatment. Eight additional rats received only the screw and were euthanized immediately after implantation. No significant effects of parathyroid hormone on body weight change or ash weight of the femurs were seen. The degree of fixation was assessed by measuring pullout strength of the screws. The mean pullout strength immediately after implantation was 12 N. The pullout strength of the group injected with saline was 33 N after 1 week, 23 N after 2 weeks, and 41 N after 4 weeks. The pullout strength of the group injected with parathyroid hormone increased to 43 N after 1 week, 58 N after 2 weeks, and 100 N after 4 weeks. The increase at 2 and 4 weeks was statistically significant. Strength reflects the mechanical properties of the bone within the screw threads. The contralateral tibia with its metal rod was used for blinded histologic assessment. Parathyroid hormone increased the fraction of the metal surface having contract with bone without an intervening soft tissue layer from 45% to 69% after 1 week. The current results suggest that intermittent parathyroid hormone treatment can enhance early implant fixation by enhancing the density of the surrounding bone and by increasing the implant bone contact.

Animals↗

PubMed2002

Insulin-like growth factor I is required for the anabolic actions of parathyroid hormone on mouse bone.

Parathyroid hormone (PTH) is a potent anabolic agent for bone, but the mechanism(s) by which it works remains imperfectly understood. Previous studies have indicated that PTH stimulates insulin-like growth factor (IGF) I production, but it remains uncertain whether IGF-I mediates some or all of the skeletal actions of PTH. To address this question, we examined the skeletal response to PTH in IGF-I-deficient (knockout [k/o]) mice. These mice and their normal littermates (NLMs) were given daily injections of PTH (80 microg/kg) or vehicle for 2 weeks after which their tibias were examined for fat-free weight (FFW), bone mineral content, bone structure, and bone formation rate (BFR), and their femurs were assessed for mRNA levels of osteoblast differentiation markers. In wild-type mice, PTH increased FFW, periosteal BFR, and cortical thickness (C.Th) of the proximal tibia while reducing trabecular bone volume (BV); these responses were not seen in the k/o mice. The k/o mice had normal mRNA levels of the PTH receptor and increased mRNA levels of the IGF-I receptor but markedly reduced basal mRNA levels of the osteoblast markers. Surprisingly, these mRNAs in the k/o bones increased several-fold more in response to PTH than the mRNAs in the bones from their wild-type littermates. These results indicate that IGF-I is required for the anabolic actions of PTH on bone formation, but the defect lies distal to the initial response of the osteoblast to PTH.

Alkaline Phosphatase↗

PubMed1982

Effect of parathyroid hormone, calcitonin and growth hormone on cAMP content of growth cartilage in experimental uraemia.

The response of proximal tibial growth cartilage cAMP content to different hormonal stimuli, i.e. parathyroid hormone, calcitonin and somatotropic hormone was evaluated in rats with bilateral or subtotal nephrectomy. In uraemic rats, basal cAMP content of growth cartilage was unchanged. Administration of 1-34 PTH in vivo or incubation of growth cartilage with 1-34 PTH in vitro caused a significantly smaller increment of cAMP in uraemic rats (40 IU PTH in vivo: 11.4 +/- 1.01 pmol cAMP/mg protein; controls 24.0 +/- 2.55; P less than 0.001). This finding implies PTH resistance. Diminished cAMP response in uraemic animals was not changed by pretreatment with 1,25(OH)2D3 or parathyroidectomy. The increment of cAMP content of growth cartilage of uraemic animals was significantly (P less than 0.01) greater after in vivo administration of 10 IU calcitonin (46.1 +/- 4.89 pmol/mg protein; control: 29.0 +/- 3.99) or incubation of cartilage with calcitonin in vitro. This finding implies overresponsiveness to calcitonin. Neither in acute nor in chronic uraemia, STH caused a significant change of cartilage cAMP or cGMP content, but STH stimulated 3H-thymidine incorporation into chondrocytes of rats with 5 days uraemia (solvent 2.98 +/- 0.51 x 10(3) cpm per cartilage; STH 5.08 +/- 0.34; P less than 0.05) and caused significant improvement of longitudinal growth of rats with 20 days uraemia.

Animals↗

PubMed2004

The physiology of the circadian rhythm of parathyroid hormone and its potential as a treatment for osteoporosis.

PURPOSE OF REVIEW: A circadian rhythm exists for parathyroid hormone, with a biphasic pattern showing a late afternoon/early evening rise and fall and a broader, longer-lasting increase late evening/early morning reaching nadir mid-morning. This review explores the characteristics of the circadian rhythm, factors regulating the rhythm and its role in bone metabolism. RECENT FINDINGS: Gender differences exist in the circadian rhythm for parathyroid hormone. Ageing in women alters the response to calcium infusion, increasing the suppression of parathyroid hormone secretion and decreasing bone resorption. There is no difference between young and elderly men in the parathyroid hormone response to calcium infusion. Loop diuretic ingestion alters the parathyroid hormone circadian rhythm reflecting loop diuretic effects on phosphate and calcium metabolism. Adult growth hormone deficiency alters parathyroid hormone secretion and end organ sensitivity, but the circadian rhythm is retained. Growth hormone replacement therapy enhances the parathyroid hormone circadian rhythm and increases end organ responses. Exogenous parathyroid hormone (1-34) and (1-84) administered by daily injection has an anabolic effect on bone, increasing bone mass and decreasing fracture. Calcilytic drugs stimulate and calcimimetic drugs suppress parathyroid hormone secretion and have been used to treat disorders of bone metabolism. SUMMARY: The circadian nature of parathyroid hormone secretion is confirmed by many publications. The underlying rhythm is endogenous. Life style factors and nutritional intake modulate the pattern of secretion. Direct association with bone resorption and formation is tentative. It is suggested that acute changes in these rhythms have little effect on resorption, but longer-term manipulation of parathyroid hormone secretion alters bone cell function. Growth hormone therapy in adult deficiency increases parathyroid hormone activity, indicating growth hormone may have therapeutic potential for osteoporosis. Manipulation of the endogenous parathyroid hormone rhythm, using timed supplements of phosphate or calcium or by calcilytic and calcimimetic molecules, offers a novel approach to osteoporosis treatment.

Adult↗

PubMed2003

The effects of parathyroid hormone and alendronate alone or in combination in postmenopausal osteoporosis.

BACKGROUND: Parathyroid hormone increases bone strength primarily by stimulating bone formation, whereas antiresorptive drugs reduce bone resorption. We conducted a randomized, double-blind clinical study of parathyroid hormone and alendronate to test the hypothesis that the concurrent administration of the two agents would increase bone density more than the use of either one alone. METHODS: A total of 238 postmenopausal women (who were not using bisphosphonates) with low bone mineral density at the hip or spine (a T score of less than -2.5, or a T score of less than -2.0 with an additional risk factor for osteoporosis) were randomly assigned to daily treatment with parathyroid hormone (1-84) (100 microg; 119 women), alendronate (10 mg; 60 women), or both (59 women) and were followed for 12 months. Bone mineral density at the spine and hip was assessed by dual-energy x-ray absorptiometry and quantitative computed tomography. Markers of bone turnover were measured in fasting blood samples. RESULTS: The bone mineral density at the spine increased in all the treatment groups, and there was no significant difference in the increase between the parathyroid hormone group and the combination-therapy group. The volumetric density of the trabecular bone at the spine increased substantially in all groups, but the increase in the parathyroid hormone group was about twice that found in either of the other groups. Bone formation increased markedly in the parathyroid hormone group but not in the combination-therapy group. Bone resorption decreased in the combination-therapy group and the alendronate group. CONCLUSIONS: There was no evidence of synergy between parathyroid hormone and alendronate. Changes in the volumetric density of trabecular bone, the cortical volume at the hip, and levels of markers of bone turnover suggest that the concurrent use of alendronate may reduce the anabolic effects of parathyroid hormone. Longer-term studies of fractures are needed to determine whether and how antiresorptive drugs can be optimally used in conjunction with parathyroid hormone therapy.

Absorptiometry, Photon↗

PubMed1991

The role of circulating N-terminal parathyroid hormone fragments in the early postparathyroid adenomectomy period.

Calcium metabolism and hormonal control after parathyroid adenomectomy are poorly understood. During the first postoperative hours, biologically active intact parathyroid hormone (PTH) (hPTH 1-84) levels are subnormal and, in spite of down-regulation of PTH peripheral receptors (caused by hypercalcemia before surgery), total and ionized calcium concentrations are maintained in the normal range. Serum samples from 20 patients with primary hyperparathyroidism were collected in the immediate preoperative period and 4 and 48 hours after excision of one parathyroid adenoma. Total and ionized calcium, intact (iPTH), midregion (mrPTH) specific PTH (hPTH 53-68), and N-terminal PTH (N-PTH) serum concentrations were determined. Levels of N-PTH were obtained with a radioimmunoassay by a modified reverse immunoextraction procedure that measures N-PTH fragments after exclusion of the interfering iPTH. No significant correlation was found between ionized and total calcium, mrPTH, and iPTH. However, total and ionized calcium levels correlated well with N-PTH (r = 0.9999, p = 0.0054, and r = 0.9993, and p = 0.0226, respectively). The data suggest that the relatively moderate decrease in calcium levels, in spite of marked decrease in circulating iPTH during the first postoperative hours, may be attributable to the minimal decrease of the bioactive N-PTH epitope concentrations. We would hypothesize that hPTH (1-34) fragments may play a significant role in regulating serum calcium levels in the early postoperative period.

Adenoma↗

PubMed2000

Distribution of parathyroid hormone-2 receptor-like immunoreactivity and messenger RNA in the rat nervous system.

The parathyroid hormone-2 receptor is a member of the secretin family of guanine nucleotide-binding protein-coupled receptors. The human parathyroid hormone-2 receptor is activated by parathyroid hormone and a recently purified hypothalamic polypeptide, tubero-infundibular peptide of 39 residues, while the rat parathyroid hormone-2 receptor is poorly activated by parathyroid hormone and is potently activated by tubero-infundibular peptide of 39 residues. In order to provide a foundation for studies on the physiological role of the parathyroid hormone-2 receptor and tubero-infundibular peptide of 39 residues, we investigated the cellular distribution of the parathyroid hormone-2 receptor in the rat CNS using both immunohistochemistry and in situ hybridization histochemistry. The receptor is found in discrete groups of neurons in many regions. It is present in scattered small cells throughout the cerebral cortex, in small and medium-sized cells in the striatum, and is quite abundant in the septum and the midline thalamic nuclei. Its expression is high in the hypothalamus, particularly in the periventricular and arcuate nuclei. Fibers and terminals in the external zone of the median eminence, and in the superficial layers of the caudal spinal trigeminal tract and the spinal cord dorsal horn, are strongly and dramatically labeled by a parathyroid hormone-2 receptor-selective antibody. The localization of parathyroid hormone-2 receptor suggests a role in the regulation of pituitary hormone secretion, sensory information processing and homeostatic regulation.

Animals↗

PubMed1991

Parathyroid hormone related protein and hypercalcaemia in breast cancer.

OBJECTIVE: To see whether parathyroid hormone related protein has a humoral role in breast cancer. DESIGN: Plasma concentrations and tumour expression of parathyroid hormone related protein were determined (by two site immunoradiometric assay and immunohistochemistry respectively) in women with breast cancer and related to the presence of bone metastases and serum calcium concentrations. SUBJECTS: Plasma concentrations of parathyroid hormone related protein were measured in 57 women with early breast cancer without apparent bone metastases, 28 women with bone metastases, and 13 women with bone metastases and hypercalcaemia. Tissue positivity for parathyroid hormone related protein was determined retrospectively in 106 primary breast tumours from women without apparent bone metastases and 72 tumours from women with bone metastases, 25 of whom subsequently developed hypercalcaemia. RESULTS: Plasma parathyroid hormone related protein concentrations were detectable (greater than 0.23 pmol/l) in 12 (92%) of the 13 hypercalcaemic patients with bone metastases compared with 10 (36%) of the 28 normocalcaemic patients with bone metastases and five (9%) of the 57 normocalcaemic patients without bone metastases. Parathyroid hormone related protein concentrations were significantly higher in hypercalcaemic than normocalcaemic patients with bone metastases. Tumour staining was positive for parathyroid hormone related protein in 22 (88%) of the 25 primary breast cancers from patients with bone metastases. Tumour staining was positive for parathyroid hormone related protein in 22 (88%) of the 25 primary breast cancers from patients with bone metastases who later developed hypercalcaemia compared with 25 (53%) of the 47 from women in this group who remained normocalcaemic and 55 (52%) of the 106 early breast cancers from women without known metastases. CONCLUSION: Tumour derived parathyroid hormone related protein may have an important humoral role in hypercalcaemia associated with metastatic breast cancer.

Bone Neoplasms↗

PubMed1993

Mechanisms underlying the regulation of parathyroid hormone secretion in vivo and in vitro.

Recent advances in our understanding of the regulation of parathyroid hormone secretion in vivo and in vitro are reviewed. The use of assays specific for immunoreactive intact parathyroid hormone has greatly improved our capacity to study parathyroid hormone dynamics in vivo. Such studies have emphasized the steep, inverse sigmoidal relationship between circulating intact parathyroid hormone and serum ionized Ca2+ concentrations, which can be modulated in a reciprocal fashion by 1,25 dihydroxyvitamin D. The use of the intact assay has also revealed additional complexities in the control of parathyroid hormone dynamics in vivo, including circadian and pulsatile patterns in parathyroid hormone as well as hysteresis and rate dependence in the relationship between intact parathyroid hormone levels and Ca2+. Studies in vitro have emphasized the role of a putative, extracellular Ca2+ receptor in regulating parathyroid function that is coupled by one or more G proteins to intracellular second messengers and parathyroid hormone secretion. Finally, the regulation of parathyroid hormone gene expression by extracellular Ca2+ and 1,25 dihydroxyvitamin D has been clarified at a molecular level by the description of specific motifs in the upstream region of the parathyroid hormone gene that mediate binding of specific inhibitory nuclear factors.

Animals↗

PubMed1982

Changes in calcium phosphate on bone surfaces and in lining cells after the administration of parathyroid hormone or calcitonin.

Small doses of parathyroid hormone and calcitonin were injected into thyroparathyroidectomized newborn rats to investigate the histological and chemical changes in bone surfaces and in mitochondrial granules of bone lining cells. Nondecalcified tissue specimens were observed under transmission electron microscope, electron probe X-ray microanalyzer, and microdiffraction after "freeze substitution" preparation of tibia shafts. Amorphous calcium phosphate, which appears as clusters and globules by this "freeze substitution" preparation, appears on the bone surfaces in a short time after the administration of a small dose of calcitonin. The Ca:PO4 ratio in the mitochondria of bone lining cells rises slightly with a small dose of parathyroid hormone and is reduced with a small dose of calcitonin. These data support the postulate that both parathyroid hormone and calcitonin act directly on bone lining cells in the process of influencing calcium concentrations of blood and temporarily storing calcium at bone surfaces.

Animals↗

PubMed1981

Analogues of an in vitro parathyroid hormone inhibitor: modifications at the amino terminus.

Four analogues of parathyroid hormone were synthesized, based on a sequence previously shown to yield an in vitro inhibitor of PTH action. Binding properties of the analogues to presumed parathyroid hormone receptors were evaluated. Each of these analogues contains a structural alteration of the amino terminus of the compound [Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide. Each of the analogues--[desamino-Ser-3, Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide, [acetyl-Glu-4, Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide, [D-Ser-3, Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide, and [pyroGlu-4, Nle-8, Nle-18, Tyr-34]bPTH-3(3-34)amide--contains modifications selected to diminish or eliminate the weak PTH-like agonist properties detected in the parent compound in vivo. To permit valid comparison of receptor-binding properties, all the analogues were derived from a common solid-phase synthesis. When assayed in the renal adenylate cyclase assay, each of the compounds inhibited completely PTH-stimulated adenylate cyclase activity and was devoid of PTH-like agonist activity. To compare the binding affinity of the analogues for parathyroid hormone binding sites, the peptides were evaluated in a parathyroid hormone renal radioreceptor assay. Each peptide demonstrated a binding affinity comparable with one another and only slightly weaker than that of the unmodified inhibitory analogue, [Nle-8, Nle-18, Tyr-34]bPTH-(3-34)amide. These studies demonstrate that it is possible to alter the amino terminus of parathyroid hormone analogues without causing a dramatic decline in affinity for the parathyroid hormone receptor. Preservation of high receptor-binding affinity in these analogues indicates that synthesis of one or several of these peptides on a scale sufficiently large to permit in vivo evaluation of both agonist and antagonist properties is warranted.

Adenylyl Cyclases↗

PubMed1972

Effect of magnesium depletion on responsiveness to parathyroid hormone in parathyroidectomized rats.

Hypocalcemia and resistance to exogenous parathyroid hormone have been reported in several clinical states associated with magnesium deficiency. On the basis of such observations, it has been suggested that magnesium depletion per se may result in impaired responsiveness of the adenyl cyclase-adenosine 3',5'-monophosphate (3',5'-AMP) system. To test this hypothesis, 4 wk old male parathyroidectomized rats were maintained on normal or magnesium-deficient diets for 4 wk and their responses to parathyroid hormone compared. Serum magnesium and calcium fell progressively in the magnesium-deficient group. Despite clinical and biochemical evidence of severe magnesium deficiency in these animals, renal production and excretion of 3',5'-AMP in response to parathyroid hormone was normal both in vitro and in vivo. Additionally, administration of either dibutyryl 3',5'-AMP or parathyroid extract to fasting magnesium-depleted rats produced a normal increase in serum calcium. Parathyroid hormone infusion studies demonstrated normal renal and skeletal responsiveness as measured by urinary excretion of calcium, magnesium, phosphate, and hydroxyproline. These data show that the effect of parathyroid hormone on 3',5'-AMP formation and excretion, the responsiveness of skeletal tissue to 3',5'-AMP, and the renal and skeletal system responses to parathyroid hormone are not altered by pure magnesium deficiency in the parathyroidectomized rat.

Adenosine Monophosphate↗

PubMed1995

Acute effect of parathyroid hormone on urine concentration in the rat.

1. It has been demonstrated that parathyroid hormone can increase adenylate cyclase activity in the rat papilla, produce a small antidiuretic effect and in vitro can interfere with the action of arginine vasopressin on water transport. Clearance studies were performed in the anaesthetized water diuretic thyroparathyroidectomized rat to evaluate further the effect of parathyroid hormone on urine concentration in the presence and absence of arginine vasopressin. 2. A maximal phosphaturic concentration of rat parathyroid hormone (2 micrograms/kg) reduced urine flow from 125 +/- 7 to 81 +/- 9 microliters/min within 10 min (P < 0.01). Addition of a maximal antidiuretic concentration of arginine vasopressin (100 ng/kg) produced a delayed and diminished antidiuretic response when compared with a group of rats not pretreated with parathyroid hormone (47 +/- 5 compared with 27 +/- 5 microliters/min; P < 0.01). However, a supramaximal arginine vasopressin concentration (1000 ng/kg) produced a maximal antidiuretic effect in the presence of parathyroid hormone. 3. To evaluate further the inhibitory effect of parathyroid hormone on arginine vasopressin-induced antidiuresis, parathyroid hormone (2 micrograms/kg) was administered to one group of rats and a minimally effective arginine vasopressin concentration (7.5 ng/kg) to another group, which produced a similar antidiuretic effect. However, the subsequent effect of a maximal antidiuretic arginine vasopressin concentration (100 ng/kg) was again significantly blunted in the group pretreated with parathyroid hormone. 4. Parathyroid hormone produced only a small increase in mean plasma calcium concentration, and glomerular filtration rate was not altered by either hormone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗