This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via Google Scholar Google Scholar Articles by GARDNER, D. G. Articles by AURBACH, G. D. Search for Related Content PubMed PubMed Citation Articles by GARDNER, D. G. Articles by AURBACH, G. D.

Prostaglandin E₂ Stimulation of Adenosine 3',5'-Monophosphate Accumulation and Parathyroid Hormone Release in Dispersed Bovine Parathyroid Cells^*

D. G. GARDNER, E. M. BROWN, R. WINDECK and G. D. AURBACH

Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health Bethesda, Maryland 20014

Address requests for reprints to: Dr. D. G. Gardner, Building 10, Room 9D-20, National Institutes of Health, Bethesda, Maryland 20014.

Abstract

Recent studies suggest that several secretagogues, in addition to calcium, may be important in the regulation of parathyroid hormone (PTH) secretion. Employing a dispersed bovine parathyroid cell system developed in this laboratory, we investigated the effects of prostaglandin E₂ (PGE₂) on the generation of cAMP and subsequent PTH release.

PGE₂ (10^-5 M) increased total cAMP (cells and medium) approximately 1.5 to 2.5-fold over the control at 15 min. This effect was not altered by (-) propranolol (10^-6 M), a-flupenthixol (10^-5 M), or phentolamine (10^-5 M). Intracellular cAMP rose to peak concentration approximately 5 min after the addition of PGE2 and extracellular cAMP increased linearly with time. Half-maximal stimulation for intracellular cAMP as well as total cAMP was observed with 10^-6 M PGE₂.

PTH release rose 75% over control at 15 min after addition of PGE₂ and was half-maximally stimulated by 3 x 10^-7 M PGE₂. PGE₂-mediated release was greatest at low calcium concentration (0.5 mM) and was suppressed by a calcium concentration of 2.0 RIM. Naproxen (10^-4 M), a potent cyclooxygenase inhibitor, did not alter the increase in PTH release after exposure to low extracellular calcium.

These results further support the possibility that intracellular cAMP is linked to PTH release and suggest a possible role for prostaglandins in the regulation of PTH secretion.

Footnotes

^* This work was presented in part at the Sixth Parathyroid Hormone Conference, Vancouver, Canada, June 12-17, 1977. It was supported in part by a grant from theKroc Foundation.

Recipient of a grant from Deutsche Forschungsgemeinschaft, N.R.

Received October 20, 1977.