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PubMed1970

Effect of thyrocalcitonin on adenosine 3':5'-cyclic phosphate formation by rat kidney and bone.

Thyrocalcitonin (TCT) increased the rate of accumulation of adenosine 3':5'-cyclic phosphate (cyclic AMP) when added to incubations containing washed particles from whole rat kidney, adenosine triphosphate (ATP), MgSO(4), and caffeine. The maximum stimulatory effect of TCT, 44 +/- 6.7 per cent, was always less than the 150 to 250 per cent increase produced by parathyroid hormone (PTH). The effect of both hormones together was no greater than that of PTH alone when each was present at a maximally effective concentration. Since neither TCT nor PTH altered the rate of degradation of cyclic AMP by the kidney preparation, it may be inferred that their effects on cyclic AMP accumulation are the result of increased formation of cyclic AMP. Adenyl cyclase activity in homogenates of renal cortex was stimulated to a greater extent by TCT and PTH than was that of medulla, whereas, as reported earlier, the effect of vasopressin was much larger with homogenates of medulla. The accumulation of cyclic AMP in incubations of rat kidney cortex slices was increased 20 to 60 per cent by TCT and 50 to 140 per cent by PTH. The accumulation of cyclic AMP in incubations of rat calvaria was increased about threefold with TCT and nine to tenfold with PTH, while reduced and alkylated TCT had less than 10 per cent of the activity of TCT. These observations are consistent with the view that the physiological effects of TCT and PTH in kidney and bone are secondary to the enhanced formation of cyclic AMP.

Adenine Nucleotides↗
PubMed1975

Clinical aspects of thyrocalcitonin.

Thyrocalcitonin (TCT) is useful as a diagnostic and therapeutic agent in selected human diseases. Elevated plasma levels of TCT occur in patients with medullary carcinoma of the thyroid gland. Asymptomatic relatives of these patients harboring microscopic foci of tumor may have abnormal plasma levels of TCT in the basal state or after provocative stimuli. In both instances the plasma levels of TCT can be used in the diagnosis and management of this thyroid neoplasm. Elevated plasma levels of TCT have also been described recently in subjects with certain extrathyroidal neoplasms or renal failure. Moderate elevations are seen during normal pregnancy and in the neonatal period. Although exogenous TCT has actions on several organs, including bone, the kidneys and the gastrointestinal tract, its physiological role in man, if any, is still unknown. The recently reported measurements of TCT in normal subjects should facilitate the clarification of this issue. TCT has been used as a therapeutic agent in Paget's disease of bone, hypercalcemia of diverse etiologies, osteopenia and several other skeletal disorders. The dramatic improvement of patients with Paget's disease has been a unique therapeutic action of TCT. The therapeutic responses in hypercalcemic subjects given TCT are encouraging but more information is needed about the pharmacology of the hormones in these subjects before conclusions can be formed. At present the therapeutic role of TCT in osteopenia is hypothetical and the results of ongoing and future studies are needed to determine its effects.

Bone Diseases↗
PubMed1976

The complete amino-acid sequence of rat thyrocalcitonin.

The complete amino acid sequence of rat thyrocalcitonin has been determined by automated Edman degradations of the intact molecule, a cyanogen bromide fragment, and by degradations of mixtures of peptides produced by hydrolysis of the hormone with trypsin and chymotrypsin. The sequence determined was H2N-Cys-Gly-Asn-Leu-Ser-Thr-Cys-Met-Leu-Gly-Thr-Tyr-Thr-Gln-Asp-Leu-Asn-Lys-Phe-His-Thr-Phe-Pro-Gln-Thr-Ser-Ile-Gly-Val-Gly-Ala-Pro-NH2. This sequence differs in only two positions from that found in the human hormone, i.e. leucine-16 in the rat vs phenylalanine-16 in the human, and serine-26 in the rat vs alanine-26 in the human. These similarities and differences are consistent with the previously reported immunological properties of the hormones isolated from these two species.

Amino Acid Sequence↗
PubMed1966

Thyrocalcitonin: cytological localization by immunofluorescence.

Thyrocalcitonin was detected in the cytoplasm of all epithelial cells of the thyroid gland of the pig, by means of antibody fluorescence. It was present in those cells whlich normally elaborate thyroglobulin but was not present in the follicular colloid.

Animals↗
PubMed1966

Thyrocalcitonin: effect on idiopathic hypercalcemia.

Identical twins having idiopathic hypercalcemia were treated with repeated doses of thyrocalcitonin extracted from porcine thyroid glands. The treatment produced a marked change in the amount of calcitum and phosphate in the plasma and in the excretion of urinary calcium.

Calcitonin↗
PubMed1969

Bone matrix turnover and balance in vitro. I. The effects of parathyroid hormone and thyrocalcitonin.

Labeled proline from incubation media has been shown to be incorporated into living bone matrix collagen in vitro. Hydroxyproline is released from fresh bone slices in similar systems in a characteristic curve against time. This hydroxyproline is derived from three distinct sources, each of which may be separately quantitated. Part of the total represents passive solubilization of matrix collagen, part is derived from new synthesis of soluble collagen occurring in vitro, and the remainder is released by cell-mediated resorptive action. The latter two processes are linear with time up to 8 hr; the former decays to zero at about 2 hr. Consequently, rates of collagen synthesis and of new collagen deposition and resorption can be quantitated simultaneously in the same system. The ability to measure these parameters of bone collagen metabolism provides methods both for the accurate evaluation of organic matrix resorption in vitro and for the accurate measurement of rates of collagen synthesis and collagen deposition. The application of the method is illustrated using parathyroid hormone and thyrocalcitonin. Parathyroid hormone diminishes collagen synthesis and stimulates collagen resorption. It reduces slightly the deposition of newly formed collagen in stable matrix. The net effect of these changes is to produce a marked negative balance. It does not significantly affect the solubility of matrix collagen.Thyrocalcitonin does not affect collagen synthesis or its deposition. It causes a marked fall in resorption rate. It has no effect on matrix collagen solubility. The net effect is to produce a marked positive balance of matrix collagen.

Animals↗
PubMed1973

Thyrocalcitonin and the jejunal absorption of calcium, water, and electrolytes in normal subjects.

Jejunal absorption of calcium, water, and electrolytes was measured in 10 normal subjects by the triple-lumen perfusion method. During the control period, water and electrolyte movements were minimal when a bicarbonate-free test solution was infused. By contrast, bicarbonate-containing solutions were readily absorbed in the control period. Intravenous infusion of synthetic salmon calcitonin (SCT) (1 Medical Research Council U/kg wt/h) over 110-120 min resulted in a marked jejunal secretion of water, sodium, potassium, and chloride in 8 of the 10 subjects. This jejunal secretion occurred with both the bicarbonate-free and the bicarbonate-containing test solutions. Calcium absorption was not affected by SCT, and the serum calcium concentration did not fall during SCT infusion. These results suggest that diarrhea in patients with medullary carcinoma of the thyroid may be due to intestinal secretion secondary to high blood concentrations of thyrocalcitonin.

Adult↗
PubMed1974

Study of the renal tubular interactions of thyrocalcitonin, cyclic adenosine 3',5'-monophosphate, 25-hydroxycholecalciferol, and calcium ion.

Acute clearance studies were performed in thyroparathyroidectomized animals to determine the actions and interactions of thyrocalcitonin (TCT), cyclic adenosine 3'5'-monophosphate (cAMP), 25-hydroxycholecalciferol (25HCC), and calcium ion on the reabsorption of phosphate, calcium, sodium, and potassium by the kidney. The infusion of 25HCC in a dosage of 60 U/h to moderately saline-expanded animals (2.5% body weight) induced a fall in the excretion of all of the ions under study after 90-120 min similar to that observed in previous experiments from this laboratory. Mean decrements in fractional excretion were: phosphate, 42.0% (P < 0.005); calcium, 25.0% (P < 0.005); sodium, 23.4% (P < 0.001); and potassium, 14.7% (P < 0.005). The superimposition of either porcine or salmon TCT (1-100 MRC U/h for 2 h) resulted in no further alterations in electrolyte excretion. However, the infusion of TCT during steady-state saline expansion, before the administration of 25HCC, obviated the renal transport effects of the vitamin D metabolite. Both in the latter studies, as well as those in which similar doses of TCT were given to hydropenic animals, the hormone itself failed to induce any consistent alteration in electrolyte excretion. Cyclic AMP (50 mg/h) caused an increase in the excretion of phosphate, sodium, and potassium and no change in calcium excretion. Like TCT, the nucleotide blocked the action of 25HCC on the kidney. Raising the mean level of serum ultrafilterable calcium to 3.02+/-0.25 mEq/liter from 1.62+/-0.17 mEq/liter likewise prevented enhanced ionic reabsorption due to 25HCC.

Absorption↗
PubMed1977

Stimulation of gastrin secretion in the pig by parathyroid hormone and its inhibition by thyrocalcitonin.

Gastrin secretion was studied in 16 young anesthetized pigs weighing 14-26 kg. Test substances were infused (0.1 ml/min x 10-20 min) directly into the gastric antrum via a catheter in the right gastroepiploic artery. Samples were collected from a catheter in the right gastroepiploic vein and plasma gastrin was measured by radiommunoassay. The following results were observed: 1) basal gastrin in antral venous blood was 10-5 times that in peripheral blood (620+/-222 pg/ml vs. 41+/-10 pg/ml, 2) native bovine parathyroid hormone (PTH) and synthetic human 1-34 PTH (0.02-4U/min) produced rapid (within 10-30 min) and pronounced (approximately 10-fold) increases in gastrin release with no increase in plasma calcium and, in several animals, in the face of a falling plasma calcium concentration, 3) neither acute thyroidectomy nor infusion of porcine thyrocalcitonin (TCT), 0.5-2.5 U/min) consistently altered basal gastrin secretion (N=3-6), and 4) infusion of TCT (0.5 U/min)along with PTH (2U/min) significantly suppressed the 10-11-fold increase in gastrin release observed when PTH subsequently was infused alone in each pig (N=6). The results demonstrate that PTH can stimulate gastrin secretion in the pig and that TCT can suppress this effect.

Animals↗
PubMed1975

Purification, characterization and radioimmunoassay of thyrocalcitonin from rat thyroid glands.

A highly purified preparation of rat thyrocalcitonin (TCT) has been obtained from lyophilized thyroid glands by gel chromatography following acid-acetone extraction. Biological activity of Sephadex G-50 eluates appeared in two peaks. The TCT in the major peak was concentrated, and applied to a Bio-Gel P-6 column, and a major protein peak was eluted which coincided with TCT activity. Potency, estimated by bioassay in rats, increase approximately 3500-fold from 0.075 MRC U/mg lyophilized glands to 250-400 MRC U/mg in the final product. The overall yield of TCT activity was about 36%. The purified product was characterized by chemical procedures and evaluated for its antigenic properties and use for radioimmunoassay. The purified rat TCT was used both labeled with 125I and as unlabeled standard. The following results were obtained: 1) Guinea pig antisera to either human or rat TCT were capable of binding 125I-rat TCT or 125I-human TCT; 2) Using either 125I-human or 125I-rat TCT and antisera to either TCT, pg amounts of rat and human TCT reacted in the assay while ng to mug amounts of salmon calcitonin or porcine TCT failed to react; 3) Using 125I-rat TCT and antisera to human or rat TCT, synthetic C-terminal (10-32 or 22-32) fragments of human TCT reacted well, while N-terminal (1-18) or desamide (1-32) derivatives reacted poorly or not at all; 4) Rat TCT was easily detected in normal thyroid venous plasma (5-10 ng/ml) and thyroid gland extracts (similar to 1 mug/gland) but not in peripheral blood; 5) Bioassay and radioimmunoassay of rat thyroid extracts (N equals 18) showed good agreement (r equals 0.86, p less than 0.001). The results support the idea that rat TCT is closely related to human TCT, indicate that major antigenic determinants reside in the C-terminal portion of the molecule, and show that antisera to either human or rat TCT can be used to measure rat TCT.

Amino Acids↗
PubMed1975

Effect of thyrocalcitonin on calcium concentration in liver of intact and thyroparathyroidectomized rats.

Thyrocalcitonin (TCT; 80 MRC mU/100g) administered SC to intact and thyroparathyroidectomized rats, caused a significant decrease in serum calcium, while increasing the liver calcium concentration. The accumulation of calcium in the liver, induced by TCT, was potentiated by the injection of calcium in both intact and thyroparathyroidectomized rats. In thyroparathyroidectomized rats, the administration of imidazole (30 mg/100 g) produced a significant increase in liver calcium and a corresponding fall in serum calcium. The rise in liver calcium produced by TCT was slightly potentiated by prior administration of imidazole, but was not enhanced by prior administration of theophylline (12 mg/100 g) which caused a significant elevation of serum calcium. These results suggest that the action of TCT on liver calcium does not involve cyclic AMP.

Animals↗
PubMed1975

Thyrocalcitonin injection to rats increases the liver inorganic phosphate.

The mechanism of the hypophosphatemic effect of thyrocalcitonin (TCT) is uncertain and may involve removal of inorganic phosphate (P1) from the plasma by heretofore unidentified organs. Rats, 192 g. thyroparathyroidectomized 16-24 h earlier, received 100 MRC mU TCT or vehicle (V) SC and 100 muCi 32PO4 iv. One h later plasma and tissue samples were collected. Compared to rats which received V, TCT-treated rats had lower plasma P1 (-0.36 plus or minus 0.08 mumol/ml, P smaller than 0.001) and Ca, higher liver P1 (+0.66 plus or minus 0.19 mumol/g, P smaller than 0.01) and unchanged red blood cell and rectus abdominus P1. TCT had no significant effect on the amount of perchloric acid soluble phosphate in any of the tissues. TCT-treated rats had lower plasma 32P1 (cpm/ml) and higher liver 32P1 (cpm/g) with no significant changes in specific activity (SA). TCT caused a small decrease in muscle 32P1 SA. There were no significant changes in the 32P (cpm/g) or 32P SA of the acid soluble phosphate fraction of any of the tissues. The results suggest that a portion of the hypophosphatemic effect of TCT can be accounted for by the increased P1 level in the liver.

Animals↗
PubMed1975

Identification of C-cells in normal and goitrous rat thyroid tissues using antiserum to rat thyrocalcitonin and the immunoperoxidase bridge technique.

Application of the immunoperoxidase bridge technique to the light microscopic localization of C-cells in rat thyroid tissue is described. Guinea pig antisera to rat thyrocalcitonin (TCT) were produced by the injection of highly purified rat TCT (100-300 MRC U/mg) emulsified in complete Freund's adjuvant. A 1:1000 dilution of the antiserum used in this study gave a strong positive reaction with rat C-cells, and 1 ml of undiluted antiserum provided sufficient material for staining approximately 5000 slides. The substitution of nonimmune guinea pig serum for the anti-rat TCT serum or the prior absorption of anti-rat TCT serum with increasing amounts of highly purified rat TCT both eliminated the staining of thyroid C-cells. Likewise, no staining was observed in tissue sections from rat parathyroid, ovary, pituitary gland, and skeletal muscle. Antiserum to synthetic human TCT also could be used to identify rat thyroid C-cells. The method revealed abundant C-cells in goiters from rats fed a low-iodine diet for more than 1 year. This finding was supported by electron microscopic evaluation of goitrous tissue and by the detection, by radioimmunoassay, of TCT in thyroid tissue and in peripheral blood from goitrous rats.

Animals↗
PubMed1976

Calcium metabolism during lactation: enhanced effects of thyrocalcitonin.

Lactating rats were compared with nonlactating controls, with regard to the intake and absorption of calcium, serum calcium level, and te protective effect of thyroacalcitonin (TC) against hypercalcemia and hyperphosphatemia. While consuming a commercial diet, intact, nonfasted lactating rats maintained a serum calcium level of approximately 9 mg/100 ml, which was 1 mg/100 ml lower than that of nonlactating controls. The level rose to that of the controls within one day after removal of the litters from the mother. Compared with nonlactating rats, lactating rats had a three-fold higher calcium intake and a six-fold higher rate of net absorption of calcium. After intragastric calcium (10 mg/100 g body wt) the increase in serum calcium was small (1 mg/100 ml) 2 h later in both groups of sham-operated rats but was markedly increased in thyroparathyroidectomized groups, with the lactating rats showing a significantly greater increase than the nonlactating rats. The injection of a small dose of porcine thyrocalcitonin completely counteracted this hypercalcemia in lactating rats, but did not have any effect on nonlactating controls. Protection by the thyroid gland against hyperphosphatemia after intragastric calcium also was significant in both lactating and nonlactating rats. The results show that TC is much more effective in lactating than in nonlactating rats, suggesting that TC may be of particular importance in lactation by restricting elevations of serum calcium and phosphorus levels after eating, thereby aiding in conservation of these ions.

Animals↗
PubMed1979

Familial hyperphosphatasemia: diagnosis in early infancy and response to human thyrocalcitonin therapy.

Familial hyperphosphatasemia is an uncommon hereditary disorder of membranous bone with concurrent overproduction and overdestruction of bone and bone collagen by osteocytes. This process does not allow normal maturation into compact lamellar bone. Two cases of severely affected children are presented which demonstrate that the condition can be diagnosed in early infancy by abnormalities in the long bones. At this stage the skull may appear normal and the characteristic thickening of the calvarium appears later. The disease is treatable with human thyrocalcitonin; these and previously reported cases have responded favorably.

Age Factors↗
PubMed1976

Improvement and initial in vivo application of the radioimmunoassay of rat thyrocalcitonin.

Previously we reported a homologous radioimmunoassy for rat thyrocalcitonin (TCT) which was sensitive enough (2--3 ng/ml serum) to measure TCT in thyroid venous blood or thyroid gland extracts but could not detect TCT in peripheral blood even after provocative challenge with iv calcium. In the present study chicken antisera to rat TCT were developed which were sufficiently sensitive (120--240 pg/ml serum) to permit initial evaluation of changes in TCT in rat peripheral blood. The following results were observed: (1) Basal serum TCT in young male Holtzman rats was undetectable, being less than 120--240 pg/ml; (2) induction of marked hypercalcemia by iv calcium increased TCT to approximately 1000--3000 pg/ml within 5 min; (3) thyroid cautery increased TCT to approximately 1000 pg/ml in 5--15 min; (4) calcium gavage (12.2 mg Ca/100 g) produced modest hypercalcemia in 30--60 min and increased serum TCT to approximately 500 pg/ml; (5) injection of isoproterenol raised serum TCT detectably; (6) injection of large doses of gastrin or pentagastrin did not produce detectable increases in TCT 5 or 30 min later. The results show that suitable antisera to rat TCT can be developed in chickens and applied to the measurement, by radioimmunoassay, of elevated circulating levels of TCT in the rat.

Animals↗
PubMedDate not supplied

[Effect of thyrocalcitonin on the pain sensitivity in animals].

With a single parenteral introduction of thyrocalcitonin (TCT) the algesthesia of soft tissues (tall skin, paw) is moderately increasing, while the algesic action of morphine and promedol against the background of TCT-gets weaker. And contrarywise algesthesia of hard tissues of the tooth becomes significantly lower under the effect of TCT and this continues for a long time.

Aminopyrine↗