Neuroendocrine Modulation of Calcitonin and Parathyroid Hormone in Man*

Abstract

Recent evidence suggests that of calcitonin (CT) and parathyroid hormone (PTH) is controlled by factors other than the ambient serum calcium concentration. We studied the effects of infusions of four neuroendocrine modulators upon CT and PTH levels: isoproterenol (beta-adrenergic agonist), methoxamine (alpha adrenergic agonist), prostaglandin E2, and somatostatin. Isoproterenol was a consistent secretagogue for both hormones. Maximal CT increments during isoproterenol infusion in normal subjects were 13 +/- 2 pg/ml (mean +/- SEM, n = 6, P less than 0.001; basal, 26 +/- 5). Maximal increments in PTH were 113 +/- 22 pg/ml (P less than 0.01, n = 6; basal, 430 +/- 11). Infusions of methoxamine increased CT by 13 +/- 5 pg/ml (n = 5, P less than 0.05; basal, 43 +/- 13), but had no effect on PTH. The means of the maximal CT increments during isoproterenol (21 +/- 8 pg/ml) and methoxamine infusion (28 +/- 11 pg/ml) were not statistically different from those achieved by acute elevations of serum calcium levels within the physiological range (41 +/- 23 pg/ml). Infusions of somatostatin and prostaglandin E2 had no or only transient effects on basal or stimulated CT or PTH levels. Our data suggest that adrenergic input modulates CT and PTH secretion in humans independently of changes in serum calcium.

Release of somatostatin-like immunoreactivity from the perfused canine thyroid. Selective stimulatory effect of calcium ions.

“…With the clear-cut inhibitory actions of somatostatin ced SLI re-in other tissues in mind, it was obvious to speculate during each that somatostatin present in the thyroid could also [ (20,22,25), whereas some have not been able to disclose any such action (18,21,23,24).…”

“…Thyroid perfusion was performed in mongrel dogs weighing [18][19][20][21][22][23][24][25][26] kg. In the dog, the two thyroid lobes are separate and can be perfused simultaneously and independently.…”

“…The evidence for an interrelationship with calcitonin release has also been controversial (18)(19)(20)(21)(22)(23)(24)(25)(26). These previous investigations have all been directed at studying an effect of administered somatostatin on the thyroid.…”

Hyperfunctioning Thyroid Adenoma Concomitant with Papillary Thyroid Carcinoma, Follicular Thyroid Adenoma and Primary Hyperparathyroidism.

“…Meanwhile, Lever et al were unable to confirm this, reporting the incidence of coexisting hyperparathyroidism to be only 0.43% [21]. It has been suggested that persistent stimulation of thyroid hormone on adrenergic receptors may lead to hyperparathyroidism [22], which is probably mediated by the induction of f3-adrenergic receptors on parathyroid cells by thyroid hormone [23][24][25]. Along with this hypothesis, Barsotti et al have reported two patients whose PTH levels returned to normal when they became euthyroid [26].…”

Effects of somatostatin on intestinal calcium absorption in man with primary hyperparathyroidism

“…This effect could be due either to unspecific actions or to a direct inhibition of the active calcium transport across the intestinal barrier (Holdsworth, 1975), the latter being mainly regulated by the active metabolites of vitamin D derived from the sequential hydroxylation of vitamin D, by the liver (Blunt, De Luca and Schnoes, 1968) and the kidney (Norman, 1974). Renal hydroxylation which results in the production of the 1,25 (OH) 2 vitamin D 3 is also controlled by calcium (Bikle and Rasmussen, 1975), phosphorus (Gray et at., 1977) and PTH (De Luca, 1978 (Metz et al, 1978). It …”