The role of adrenergic stimuli in the secretion of parathyroid hormone (PTH) in man was evaluated. Intradermal injections of isoproterenol, 0.15 mg, or epinephrine, 0.3 mg, caused significant prompt increases in serum PTH levels. These increases were not accompanied by any changes in serum calcium (Ca) during the period of observation. Phenylephrine, 1.5 mg, intradermally, did not cause any significant changes in serum PTH or serum Ca. Propranolol infusion alone significantly inhibited the basal secretion of PTH. This inhibition by propranolol was overcome by isoproterenol administration. The results indicate that 1) beta adrenergic agents increase PTH secretion whereas alpha adrenergic agents have no effect, 2) beta adrenergic stimuli probably play an important physiological role in basal PTH secretion in man.

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Estrogen therapy has been used to inhibit bone resorption and prevent osteoporosis in postmenopausal women. Previous studies have disagreed as to whether the mechanism of estrogen action involves stimulation of calcitonin (CT) secretion. We evaluated the direct effects of 17 beta-estradiol (E2) and progesterone (Prog) on CT secretion from the thyroid C cells of 8-day-old rats in vitro. Both E2 and Prog caused a significant stimulation of CT secretion within 1 h, which was progressive for the 3-h observation period. The responses were dose related from 10(-7) to 5 X 10(-10) M. There was no CT response to 10(-7) M alpha-estradiol, estriol, 3-methoxyestriol, estrone, testosterone, or 20 alpha-hydroxyprogesterone, indicating specificity of the responses to E2 and Prog. There was a minimal CT secretory response to 10(-6) M cortisol. The E2 receptor antagonist tamoxifen did not inhibit the E2 effect on CT secretion. This observation plus the rapid CT response suggest that this hormonal effect may not be via the conventional intracellular E2 receptor. Therefore, E2 and Prog can stimulate CT secretion by rapid, direct, and specific effects on the thyroid C cell. The gonadal hormones may, therefore, be important in inhibiting bone resorption via their direct stimulatory effect on CT secretion.

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Excessive glucocorticoids can cause osteopenia in animals ( 1 ) and man (2). However, the mechanisms by which they produce this effect are not entirely clear. In vitro studies have shown that glucocorticoids inhibit vitamin A or parathyroid hormone (PTH)-induced bone resorption (3). In vivo studies have shown that glucocorticoids inhibit bone formation (4, 5 ) . However, the bone resorption studies in vivo have given conflicting results (5,6). In studies which showed increased bone resorption due to glucocorticoids, excessive PTH has been postulated as one of the mechanisms of this increase. Excessive PTH secretion has been shown to occur in rats (7) and in man (8) after acute or chronic cortisol administration.Recent studies have indicated that the glucocorticoids' effect on bone resorption may be dose-dependent , low doses causing increased resorption and high doses causing decreased or normal resorption (9, 10). The increased bone resorption was again postulated to be the result of excessive PTH secretion.The present studies were conducted to evaluate the role of parathyroid glands in the production of glucocorticoid-induced osteopenia.Materials and Methods. Sprague-Dawley rats initially weighing 260-290 g were maintained on a diet containing 1.7% calcium and 1.5% phosphorus. All rats were injected with 45 pCi of 4*5Ca ip in three divided doses at 3-day intervals. Ten days ~~ ' Note: This work was presented in part at the Annual Meeting of the Midwestern Section of the American Federation for Clinical Research on October 31, 1974, Chicago, Illinois. Address reprint requests to: Subhash C. Kukreja, M. D., VA West Side Hospital (M. P. 172), P. 0. Box 8 195, Chicago, Illinois 60680.after the last dose of 4*5Ca, half the rats were parathyroidectomized (PTX) and the other half were left intact. Parathyroidectomy was confirmed by serum calcium levels of less than 7.0 mg/l00 ml and undetectable serum PTH levels.The animals were divided into four groups 1 week after the parathyroidectomy, at which time injections were begun and continued daily for 17 weeks. Group I: Intact rats were given normal saline sc daily to serve as control ( n = 6). Group 11: Intact rats were given cortisol (Cortef, Upjohn Company, Kalamazoo, Mich .) , 5 mg/kg/day sc (n = 6). Group 111: PTX rats were given normal saline sc daily (n = 5 ) . Group IV: PTX rats were given cortisol, 5 mg/kg/day sc (n = 4).The rats were kept in individual metabolic cages. The animals were bled by orbital sinus puncture at 2 weeks, 12 weeks, and at the end of the study at 17 weeks. The serum was separated and analyzed immediately for 4 T a activity and frozen for subsequent determinations of calcium, phosphorus, and PTH.Two weeks after beginning the injections, the feces were collected for two successive 72-h periods and then ashed. The ash was dissolved in hydrochloric acid for analysis of 4 T a activity.At the end of 17 weeks the rats were killed by ether anesthesia and the right femur was removed. The bone was quickly freed of soft tissue and weighed. The lengt...

This study evaluated the effect of somatostatin on immunoreactive parathyroid hormone (iPTH) and calcitonin (iCT) secretion in vivo in rats and monkeys and on iPTH secretion in vitro by normal bovine parathyroid tissue and by a human parathyroid adenoma. Somatostatin infusion promptly (within 0.5 h) suppressed both iPTH and iCT in both species studied in vivo, the suppression being progressive during the infusion period. In in vitro studies, somatostatin caused significant dose-related decreases in basal, low Ca-stimulated, and high Ca-suppressed PTH secretion from normal bovine parathyroid tissue and from basal and low Ca-stimulated PTH secretion from a human parathyroid adenoma. Therefore, somatostatin 1) suppresses both PTH and CT secretion in vivo; 2) acts directly on the parathyroid cell and presumably directly on the C-cell also; 3) acts upon normal and adenomatous parathyroid tissue; 4) suppresses basal, low Ca-stimulated and high Ca-suppressed PTH secretion; and 5) has a dose-related effect. The possible role of somatostatin in the physiological control of PTH and CT secretion (and therefore in Ca homeostasis), and in the pathogenesis of abnormalities of Ca homeostasis, requires further evaluation.