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β-Adrenergically Stimulated Adenosine 3',5'-Monophosphate Accumulation in and Parathyroid Hormone Release from Dispersed Human Parathyroid Cells^*

EDWARD M. BROWN, DAVID G. GARDNER, RAJNER A. WINDECK, SAMUEL HURWITZ, MURRAY F. BRENNAN and GERALD D. AURBACH

Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases (E.M.B.,D.G.G., R.A.W., S.H., G.D.A.), and the Surgery Branch, National Cancer Institute (M.F.B.), National Institutes of Health, Bethesda, Maryland 20014

The effects of β-adrenergic agonists on cAMP accumulation and parathyroid hormone (PTH) release were studied with dispersed human parathyroid cells from adenomatous and primarily hyperplastic tissue. (–)Isoproterenol stimulated intra- and extracellular cAMP in a dose-dependent fashion, and this effect was stereospecifically inhibited by (–)- and (+)propranolol. Moreover, β-adrenergic receptors were directly identified with the high affinity, high specific activity β-adrenergic antagonist [^l25I]hydroxybenzylpindolol. (-)Isoproterenolstimulated cAMP accumulation in cell preparations from individual pathologic glands varied from 0-12 pmol/10⁵ cells. PTH release was also stimulated 0-140% by 10⁶ M (-)isoproterenol. There was not a clear correlation, however, between maximal β-adrenergically stimulated cAMP content and PTH release in different cell preparations, suggesting that factors in addition to intracellular cAMP content per se determined the magnitude of hormone release. In some instances, the β-adrenergically mediated secretory response may have been inhibited by elevated extracellular calcium concentration. In addition to quantitative variation in β-adrenergic response, individual cell preparations varied in the type of β-receptor present. In eight instances, responses were characteristic of β₁-receptors, while in eight others, responses were of the β₂ type. cAMP accumulation was also stimulated 2.5- to 100-fold by glucagon, prostaglandin E₂, or histamine, while neither secretin nor dopamine caused much, if any, effect. These results suggest that dispersed cells from pathologic parathyroid tissue are capable of responding to a variety of agonists, but that there is quantitative as well as qualitative variation among cell preparations from individual patients. (J Clin Endocrinol Metab 48: 618, 1979)

^* This work was supported in part by a grant from the Kroc Foundation.

Supported by a grant from the Deutsche Forschungstemeinschaft (N.R. Wi 507/1 and 2). Present address: 30 Morikestr, 403 Ratingen-Lintorf, West Germany.

Present address: Agricultural Research Organization, The Volcani Center Institute of Animal Sciences, P.O. Box 6, Bet Dagan 50-200, Israel.

Received June 14, 1978.

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