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Biomedical subjects

L Gozariu

Publications and source records attributed to L Gozariu.

At least 55 records · Page 3Linked to original sources
PubMedDate not supplied

The role of some activators and inhibitors of calcium channels on the dynamics of serum magnesium.

Magnesemia was determined in male rats weighting 120 +/- 10 g after intravenous administration of nifedipine, an antagonist of calcium channels, and BAY-K 8644, an activator of calcium channels. Nifedipine does not alter the basal level of serum Mg 30 minutes after administration in normal animals or in animals in which chemical sympathectomy was induced by administration of 6 OH-dopamine. On the other hand, BAY-K 8644 induces a significant rise of basal magnesemia from 2.1 +/- 0.2 mg% to 2.7 +/- 0.1 mg% in normal animals. In animals sympathectomized with 6 OH-dopamine, their rise is maintained at about the same level from 2.0 +/- 0.1 mg% after administration). Propranolol previously administered inhibits the stimulating action induced by the calcium channel agonist, BAY-K 8644.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
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Calcitonin reserve and the differentiated response to calcitonin in osteoporosis.

The authors followed up the effect of calcium and calcitonin administration on phosphorus-calcium balance and on calcium retention, in correlation with the level of endogenous calcitonin, in 20 patients of perimenopause age (40-50 years), with radiologically confirmed osteoporosis. Calcium retention after loading with calcium gluconate (180 mg in i.v. injections) was determined before and after administration of salmon calcitonin (100 IV in i.m. injections). Two types of responses were noted. In a group of patients calcitonin administration determined a rise of calcium retention at the same time with the improvement of other biochemical parameters as well as a normal calcitonin response. The presence of high levels of circulating calcitonin 24h after loading with exogenous calcitonin demonstrated a slower inactivation rate of the hormone in these patients. The other group showed no positive response to calcitonin. The proposed test is a criterion for the selection of the patients with osteoporosis in view of chronic calcitonin treatment.

Adult↗
PubMedDate not supplied

Stimulation of calcitonin secretion by beta-calcitonin gene related peptide in rats.

The presence of calcitonin gene-related peptide (CGRP) in both C-cells and nerve fibres around the thyroid blood vessels and follicles suggests that it may play a dual role, one of which may be in hormone secretion. Beta-CGRP injected intracerebroventricularly (icv) (1.875 nmol) caused a significant increase in the calcitonin CT) content of the C-cells in rat thyroid glands. The calcitonin content of the thyroids was determined by a radioimmunoassay using two antibodies and the results were expressed as ng CT/mg of fetal tissue. A significant rise in CT content of the thyroids occurred (5.5 +/- 0.5 n = 6), compared with the controls (3.5 +/- 0.1 n = 6). It is presumed that this change reflects an increase in the rate of secretion of CT in the thyroid glands of those rats so treated. The peptide might act on the central nervous system to stimulate the catecholamine outflow from the thyroid nerves and thereby increase the secretion rate of CT.

Animals↗
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Effect of "APUD"-type hormones on osteolysis in vitro.

Besides their well-known actions, glucagon, ACTH, pentagastrin and insulin from the APUD series exert a direct action on the bone calcium content. Incubation with these substances of rat calvaria in vitro yields an evident stimulation of osteolysis with ACTH. Pentagastrin inhibits osteolysis. Glucagon and insulin inhibit parathormone-stimulated osteolysis, with no influence on the spontaneous one. Glucagon, resembling calcitonin, stimulates the 45Ca uptake from the incubation medium. The action of these substances completes the series of hormones influencing bone calcium metabolism, underlining possible interference actions of APUD-type hormones.

APUD Cells↗
PubMedDate not supplied

Stimulating effect of calcium channel activator BAY-K 8644 on calcitonin secretion.

The calcium channel activator BAY-K 8644 injected intravenously produces a significant rise in the calcitonin content of the thyroid. Because adrenalin and noradrenaline play a certain role in the regulation of ionic calcium channels and in the preservation of the secretory tonus of the calcitonin secreting C cells, the effect of BAY-K 8644 was followed-up in adrenalectomized animals and in animals in which propranolol was previously administered. Adrenalectomy of beta receptor blocking does not prevent the effect of BAY-K 8644 on the activation of calcium channels, the calcitonin secretion being stimulated in these conditions too. The data obtained stress the relative independence of the calcium channels or the beta-adrenergic stimulating system in the achievement of calcium ion transfer. However, the calcitonin levels obtained were lower in adrenalectomized animals or following propranolol after stimulation with BAY-K 8644 in those with intact sympatho-adrenergic tonus. This stresses the importance of the integrity of the beta receptors in the activation of the calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Parathormone and calcitonin secretion in endemic goiter.

The investigations performed on 160 females of adult age with goiter and clinical signs of spasmophilia followed up the serum and urinary calcium and magnesium. The calcitonin and parathormone circulating levels were also determined. Although the levels of serum and urinary calcium and magnesium appear normal in adult subjects with simple goiter, decreased levels of the circulating parathormone were confirmed in most cases. The values of circulating calcitonin were within normal limits. The moderate hypoparathyroidism noted is an indication of the possible association of "parathyroid dystrophy" with endemic goiter.

Adult↗
PubMedDate not supplied

Effect of calcitonin on phosphorylase a and glucose-6-phosphatase activities in the hepatic particulate glycogen of rats.

A single dose of calcitonin (CT) (70 mU MRC/100 g body weight) was administered in 50 and 90 days old male Wistar rats. In both ages CT determined a rise of Phosphorylase a and glucose-6-phosphatase activity as well as an increased calcium accumulation at the level of liver particulate glycogen. In the rats receiving CT glycemia increased and the liver glycogen content decreased. With the exception of liver glycogen the other metabolic parameters studied were modified at the two ages in the same manner under the influence of the same dose of CT.

Animals↗
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Changes in calcitonin secretion and in serum magnesium following adrenalectomy in rats.

The level of serum magnesium and also thyroid of calcitonin content was followed up in the conditions of adrenalectomy after hydrocortisone replacement as well as after calcium propranolol administration. Six days after adrenalectomy a significant decrease both of calcitonin secretion and of serum magnesium was noted. Hydrocortisone replacement reestablished the levels of both parameters to the levels found in controls. Adrenalectomy also reduced the calcitonin secretory response consequent to calcium loading, but calcium excess simultaneously determined hypermagnesemia. Propranolol, a beta blocker with direct action on the secretory tonus of the thyroid C cells, completely annulled the stimulation effect of calcium in adrenalectomized animals but not the hypermagnesemic response. The adrenocortical hormones interfere in the calcitonin-magnesium secretory antagonism, together with the sympathetic -adrenergic system, ensuring the secretory control of calcitonin especially by blocking the occurrence of an excess of magnesium which reduces calcitonin secretion.

Adrenal Cortex↗
PubMedDate not supplied

Calcitonin secretion in rats with inflammation mediated osteopenia.

The authors followed up the occurrence of inflammation-mediated osteopenia (IMO) in young and adult rats weighing 50 g and 150 g, respectively. The calcemia, the amount of bone calcium and the calcitonin content of the thyroid gland were determined. Calcium loss from bones was similar in both groups, irrespective of age. However, in the young animals a significant rise of calcitonin content of the thyroid gland was found (11.08 ng/ml as compared with 3.81 ng/ml in the controls). In adult animals with IMO the level of calcitonin in the thyroid gland showed no change as compared with the controls. Calcitonin reactive hypersecretion in the young animals was not able to prevent the development of IMO, characterized by an important loss of bone calcium.

Aging↗
PubMedDate not supplied

The effect of some enkephalins on calcitonin secretion.

Synthetic enkephalins: 5 metenkephalin, D2 proenkephalin and 5 leuenkephalin and morphine were injected into cerebral ventricles of rats. After 30 minutes the rats were sacrificed and the calcitonin content of the thyroid was assayed. As compared to the controls, morphine reduced significantly the secretion of calcitonin. Of the enkephalins, only 5 leuenkephalin had a borderline effect on calcitonin secretion, stimulating to a significant degree the rise of the hormone. The data obtained demonstrate the selective effect of opiates on calcitonin secretion.

Animals↗
PubMedDate not supplied

Reactivity to calcitonin after ovariectomy.

The hypocalcemic response to calcitonin injected in female rats disappeared after their castration. The substitution treatment with estrogens does no allow reestablishment of the hypocalcemic effect obtained in intact animals, a fact that lays stress on the role of the whole ovarian secretion in maintaining a normal response to calcitonin. The response of castrated animals to calcitonin calls attention to the conditional role of estrogens in validating the osteoprotecting effect of calcitonin.

Animals↗