Inhibitory role of somatostatin on calcitonin secretion.

Calcitonin (CT) secretion is not exclusively controlled by calcemia, but the secretory tonus is maintained by the beta-stimulatory adrenergic system Somatostatin (SMS) plays a neuromodulatory role with the reduction of CT secretion by its interference at the central and peripheral level of the beta adrenergic receptors. The experiments were carried out on groups of rats in which the effect of SMS on CT content of the thyroid gland was followed up. Thus, SMS administered i.c.v. significantly reduced the basal CT secretion without blocking the stimulatory effect of calcium. The results were comparable with those obtained after the blockade of the sympatho-adrenergic system by chemical sympathectomy with 6HODA or propranolol. Central blockade of alpha receptors with phentolamine determined a significant rise of CT. This effect was annihilated by SMS. The i.v. administration of SMS did not induce a change in CT content of the thyroid, but blocked the stimulatory action of hypercalcemia. The results are identical with those obtained by blocking the beta-receptors with propranolol. SMS also blocked the stimulatory effects of isoproterenol on CT secretion. The data obtained revealed the fact that SMS lowers CT secretion by the central and peripheral interference of the sympatho-adrenergic path, maintaining the secretory tonus of the thyroid C cells.

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.

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.

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.