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Biomedical subjects

H Pavlovitch

Publications and source records attributed to H Pavlovitch.

12 recordsLinked to original sources
PubMed1980

Lack of effect on ovariectomy on the metabolism of vitamin D and intestinal calcium-binding protein in female rats.

The metabolism of 25-hydroxycholecalciferol (25-(OH)D3), plasma concentration of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and the amount of calcium-binding protein (CaBP) in duodenal mucosa were determined in ovariectomized rats and were compared with data observed in normal age-matched cyclic rats. Sephadex LH-20 and high-pressure liquid chromatography were used for the study of the metabolism of 25-(OH)D3. The concentration of 1,25-(OH)2D3 in plasma and prolactin in serum were measured by radioimmunoassay. Calcium-binding protein in duodenal mucosa was determined immunologically using electroimmunodiffusion. The results showed that the lack of ovarian hormones and low prolactin levels observed in ovariectomized rats did not promote a significant change in the metabolism of 25-(OH)D3, in the levels of 1,25-(OH)2D3 in the circulation or in the amount of CaBP in duodenal mucosa. It is possible that the regulation of 25-(OH)D3 by sex hormones is restricted to the state of calcium stress such as during egg-laying in birds or pregnancy and lactation in mammals.

Animals↗
PubMed1978

Effect of growth hormone on the metabolism of 25-hydroxycholecalciferol in hypophysectomized rats on a diet without vitamin D and low in calcium.

The metabolism of 25-hydroxycholecalciferol (25-(OH)D3) was investigated in rats fed a diet low in calcium and without vitamin D for 4 weeks after hypophysectomy. Compared with intact rats on the same diet these animals had a low serum phosphorus concentration, a less marked degree of hypocalcaemia and their parathyroid gland was not hypertrophied. Eighteen hours after i.p. injection of a single dose of tritiated 25-(OH)D3, chromatography of serum extracts on Sephadex LH-20 showed that the percentage of radioactivity corresponding to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) was lower in hypophysectomized rats than in control rats. High-pressure liquid chromatography demonstrated that 81% of this material had the same elution profile as 1,25-(OH)2D3. The percentage of 1,25-(OH)2D3 in the serum of hypophysectomized rats could be increased to the level seen in the controls by chronic treatment with bovine growth hormone. This action of growth hormone was most probably independent of the parathyroid glands since the injection of parathyroid extract did not alter 25-(OH)D3 metabolism in hyophysectomized animals. These results suggest that the decrease in the conversion of 25-(OH)D3 to 1,25-(OH)2D3 after hypophysectomy may be related to the lack of growth hormone.

Animals↗
PubMed1977

Maintenance of a calcemic response to parathyroid hormone in D-deficient rats by the prevention of severe hyperparathyroidism.

Parathyroid gland transplanted rats and hypophysectomized rats were raised from weaning on a diet without vitamin D and low in calcium (0.02%) for 4 weeks. At the enn of this period the animals of both experimental groups, when compared to their respective controls (i.e., sham-operated animals for parathyroid-transplanted ones, and hypophysectomized plus bovine growth hormone-supplemented ones for hypophysectomized rats) were characterized by (a) moderate or absent secondary hyperparathyroidism; (b) near normal bone calcium content; and (c) a maintained responsiveness to the calcemic effect of parathyroid extract (PTE). The PTE action is a bone effect that does not require the presence of the kidneys and is not related to changes in serum calcium and/or phosphorus concentrations. These results indicate that when severe hyperparathyroidism is prevented, the sensitivity of bone to the calcemic action of PTE can be maintained in D-deficient calcium-deprived rats. They also suggest that in these animals the main factor leading to resistance to PTH is the state of severe chronic hyperparathyroidism.

Animals↗
PubMed1977

Decreased bone sensitivity of thyroidectomized rats to the calcaemic effect of 1,25-dihydroxycholecalciferol.

The calcaemic response of thyroidectomized parathyroid transplanted rats to a single dose of biosynthetic 1,25-dihydroxycholecalciferol (50 ng) injected into a jugular vein, was evaluated. The animals were fed a vitamin D-free, low calcium diet. Compared to sham-operated and to thyroid-intact parathyroid transplanted rats thyroidectomized animals had a significantly reduced calcaemic response to 1,25-dihydroxycholecalciferol. Daily supplementation with d,1-thyroxine (100 mug/rat) during the experimental period restored a normal response. The increase in serum calcium concentration after 1,25-dihydroxycholecalciferol injection was a similar in thyroidectomized bilaterally nephrectomized animals, and in thyroidectomized kidney-intact rats. The results suggest that in thyroxine depleted rats, the sensitivity of bone to the calcaemic effect of 1,25-dihydroxycholecalciferol is decreased.

Animals↗
PubMed1976

1,25-Dihydroxycholecalciferol increases bone resorption in thyroparathyroidectomised mice.

Mice, 1 week old, prelabelled with 45Ca, were either thyroparathyroidectomised or sham-operated; 1 day later half of the mice of each group were injected with 1,25-dihydroxycholecalciferol (5 ng/g), and 20 h later all the mice were killed. Bone resorption in explants was then measured by an in vivo/in vitro technique previously published; compared with untreated mice it was found that 1,25-dihydroxycholecalciferol had increased resorption irrespective of whether the mice had been thyroparathyroidectomised or not. These data suggest that 1,25-dihydroxycholecalciferol is able to increase bone resorption independently of parathyroid hormone.

Animals↗
PubMed1976

Maintenance by cortisone of the calcemic response to parathyroid extract of rats on a diet without vitamin D and low in calcium.

Weanling rats raised for 21 days on a vitamin D deprived, low Ca diet (0.02%), and given chronic cortisone administration (5 mg/kg/d), maintain responsiveness to the hypercalcemic effect of endogenous and exogenous parathyroid extract (PTE). The PTE action is a bone effect that does not require the presence of the kidneys, and is not related to a higher concentration of calcium or cortisone. Maintained sensitivity of D- Ca- Cort+ rats to PTE does not appear to be the consequence of a lesser degree of D-deficiency: the whole body vitamin D pool and its chloroform-soluble fraction in these animals are not different from those of their D- Ca- PTE- unresponsive controls. Repeated PTE injections for 4 days exhaust the sensitivity to the hypercalcemic action of PTE of D- Ca- Cort+ rats. The present data seem to indicate that cortisone-treated D- Ca- rats, responsive to the bone action of PTE, are characterized by a near normal bone calcium content and Ca/P ratio, and a significant increase in the number of osteoclasts.

Animals↗
PubMed1974

Metabolism of 25-hydroxyvitamin D3 in anephric rats: a new active metabolite.

After the injection of radioactive 25-hydroxyvitamin D(3) into rats given a normal diet, two metabolites can be detected on Sephadex LH-20 chromatography modified to reveal polar metabolites. The first is designated peak Va, which by means of periodate cleavage has been identified as 24,25-dihydroxyvitamin D(3). The second more polar metabolite has been designated peak X(1) and is only partially sensitive to periodate. This metabolite appears in serum, bone, intestine, and liver and does not chromatograph on any system like any of the previously identified metabolites. Nephrectomy, especially in the animals given large doses of 25-hydroxyvitamin D(3), does not abolish production of either peak Va or X(1), revealing that both metabolites can be made in extra-renal tissue. Peak X(1) has marked ability to elevate serum calcium of rats on a vitamin D-deficient, low calcium diet, but requires the presence of kidneys to carry out this function.

Animals↗
PubMed1973

Calcium-mobilizing effect of large doses of 25-hydroxycholecalciferol in anephric rats.

The effect of high doses of 25-hydroxycholecalciferol on plasma calcium concentration was studied in rats receiving a low-calcium normal vitamin D diet. In bilaterally nephrectomized animals, as in sham-operated controls, 62.5 nmol of 25-hyroxycholecalciferol did not produce a rise of plasma calcium concentration. In contrast, the administration of 125 or 625 nmol, doses 1,000-5,000 times the minimal active dose in D-deficient rats, was followed in both groups of animals by a significant increase of plasma calcium concentration. Removal of either parathyroids alone or parathyroid and thyroid glands did not suppress this effect. These data suggest that when large doses are used in vivo, the renal conversion of 25-hydroxycholecalciferol to more polar metabolites is not an obligatory step for its calcium-mobilizing action. The present study does not elucidate, however, the exact mechanism(s) of this effect.

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