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β-adrenergically stimulated adenosine 3', 5'-monophosphate accumulation in and parathyroid hormone release from dispersed human parathyroid cells
Year:
1979
Authors :
Hurvitz, Shmuel (Animal science)
;
.
Volume :
48
Co-Authors:
Brown, E.M., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Gardner, D.G., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Windeck, R.A., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Hurwitz, S., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States, Agricultural Research Organization, Volcani Center Institute of Animal Sciences, P.O. Box 6, Bet Dagan, 50-200, Israel
Brennan, M.F., Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20014, United States
Aurbach, G.D., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Facilitators :
From page:
618
To page:
626
(
Total pages:
9
)
Abstract:
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 [125I]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 10‑6 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. © 1979 by The Endocrine Society.
Note:
Related Files :
bucladesine
cell membrane
Cyclic AMP
human cell
iodohydroxybenzylpindolol i 125
Parathyroid Glands
propranolol
secretin
Show More
Related Content
More details
DOI :
10.1210/jcem-48-4-618
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
22095
Last updated date:
21/08/2022 07:45
Creation date:
16/04/2018 23:49
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Scientific Publication
β-adrenergically stimulated adenosine 3', 5'-monophosphate accumulation in and parathyroid hormone release from dispersed human parathyroid cells
48
Brown, E.M., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Gardner, D.G., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Windeck, R.A., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Hurwitz, S., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States, Agricultural Research Organization, Volcani Center Institute of Animal Sciences, P.O. Box 6, Bet Dagan, 50-200, Israel
Brennan, M.F., Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20014, United States
Aurbach, G.D., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
β-adrenergically stimulated adenosine 3', 5'-monophosphate accumulation in and parathyroid hormone release from dispersed human parathyroid cells
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 [125I]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 10‑6 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. © 1979 by The Endocrine Society.
Scientific Publication
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