Effect of parathyroid hormone and thyrocalcitonin on various pathogenetic mechanisms of duodenal ulcer
Mosin, V.I.; Drzhevetskiĭ, I.M.; Iagoda, A.V.; Gumunskaia, T.P.; Grosman, B.E.
Terapevticheskii Arkhiv 52(11): 73-77
1980
ISSN/ISBN: 0040-3660 PMID: 6258257 Document Number: 161555
The stomach secretory function, the blood levels of cAMP and cGMP, Ca, P, insulin, glucagon and gastrin determined before and after giving parathyroid hormone and thyrocalcitonin to patients with duodenal ulcers, were examined. These levels, as well as the blood levels of parathyroid hormone and calcitonin, were determined in response to i.v. injection of calcium gluconate. Parathyroid hormone produced a stimulatory effect on the basal acid production and did not influence histamine-stimulated gastric secretion. Thyrocalcitonin produced a pronounced inhibitory effect on the basal and the histamine-stimulated acid production. The injection of calcium gluconate inhibited the endogenous secretion of parathyroid hormone, but did not influence the production of calcitonin. The principal action of the hormone on parietal cells consisted of a reduction of cGMP synthesis, while thyrocalcitonin reduced the synthesis of cAMP. Parietal cells are evidently the site of application of the parathyroid hormone and thyrocalcitonin action. Their specific contact with the regulatory subunits of cyclases is the key mechanism of their characteristic influence on cell metabolism and HCl production. Extracellular Ca produces an indirect effect on the function of the parietal cells by impeding the release of the parathyroid hormone and subsequent change of Ca ion transport across the membranes. The direct action of parathyroid hormone and thyrocalcitonin on the secretion of pancreatic hormones and gastrin release is negligible; this action may be an indirect one (via changing the circulation of systemic nucleotides).