חיפוש מתקדם
Endocrinology
Brown, E.M., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Hurwitz, S.H., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, 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
The possibility of α-adrenergic modulation of cAMP accumulation and parathyroid hormone (PTH) release was investigated in dispersed bovine parathyroid cells. cAMP accumulation due to the mixed α- and β-adrenergic agonists, (-)epinephrine and (-)norepinephrine, was significantly enhanced by the α-adrenergic inhibitor phentolamine; that due to the “pure”β-adrenergic agonist, (-)isoproterenol, was not altered significantly. Direct inhibition of agonist-stimulated cAMP accumulation was effected by adding increasing concentrations of (-)epinephrine to concentrations of (-)isoproterenol maximally stimulating cAMP accumulation. A 50–75% inhibition of cAMP was observed which was specifically blocked by phentolamine. This inhibition was not specific for β-adrenergic stimulation, as (-)epinephrine also inhibited dopamine-stimulated cAMP accumulation. The inhibition of (-)isoproterenol- stimulated cAMP accumulation by (-)epinephrine was unaffected by ambient calcium concentration. Stimulation of PTH release by (-)epinephrine and (-)norepinephrine was potentiated by phentolamine and inhibited by the β-adrenergic blocker, (-)propranolol, demonstrating α-adrenergic modulation of hormone release and confirming the close relationship between cAMP accumulation and PTH release previously shown in this system. These results demonstrate the presence of an α-adrenergic receptor in dispersed bovine parathyroid cells which inhibits agonist-stimulated cAMP accumulation and PTH release by a mechanism independent of extracellular calcium. © 1978 by The Endocrine Society.
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תנאי שימוש
α-adrenergic inhibition of adenosine 3′, 5′-monophosphate accumulation and parathyroid hormone release from dispersed bovine parathyroid cells
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Brown, E.M., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, National Institutes of Health, Bethesda, MD, 20014, United States
Hurwitz, S.H., Metabolic Diseases Branch, National Institute of Arthritis, Metabolism, and Digestive Diseases, 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
α-adrenergic inhibition of adenosine 3′, 5′-monophosphate accumulation and parathyroid hormone release from dispersed bovine parathyroid cells
The possibility of α-adrenergic modulation of cAMP accumulation and parathyroid hormone (PTH) release was investigated in dispersed bovine parathyroid cells. cAMP accumulation due to the mixed α- and β-adrenergic agonists, (-)epinephrine and (-)norepinephrine, was significantly enhanced by the α-adrenergic inhibitor phentolamine; that due to the “pure”β-adrenergic agonist, (-)isoproterenol, was not altered significantly. Direct inhibition of agonist-stimulated cAMP accumulation was effected by adding increasing concentrations of (-)epinephrine to concentrations of (-)isoproterenol maximally stimulating cAMP accumulation. A 50–75% inhibition of cAMP was observed which was specifically blocked by phentolamine. This inhibition was not specific for β-adrenergic stimulation, as (-)epinephrine also inhibited dopamine-stimulated cAMP accumulation. The inhibition of (-)isoproterenol- stimulated cAMP accumulation by (-)epinephrine was unaffected by ambient calcium concentration. Stimulation of PTH release by (-)epinephrine and (-)norepinephrine was potentiated by phentolamine and inhibited by the β-adrenergic blocker, (-)propranolol, demonstrating α-adrenergic modulation of hormone release and confirming the close relationship between cAMP accumulation and PTH release previously shown in this system. These results demonstrate the presence of an α-adrenergic receptor in dispersed bovine parathyroid cells which inhibits agonist-stimulated cAMP accumulation and PTH release by a mechanism independent of extracellular calcium. © 1978 by The Endocrine Society.
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