High plasma levels of catecholamines during insulin-induced hypoglycemic stress do not cause β-adrenergic receptor sequestration

F. Negri, M. Fratelli, P. Fratino, G. M. D'Eril, G. Finardi, A. De Blasi

Research output: Contribution to journalArticle

Abstract

In the present investigation insulin-induced hypoglycemia was used as a powerful stimulus to rapidly release epinephrine from the adrenal medulla. Insulin injection raised epinephrine 16-fold and doubled norepinephrine plasma levels. The aim of this attempt was to induce β-adrenergic receptors (β-ARs) sequestration in vivo on mononuclear leukocytes (MNLs). The number of total and surface β-ARs was significantly increased 30 minutes after insulin administration, with only partial recovery at 90 minutes. No detectable receptor sequestration was observed: surface receptors were about 90% of total receptors in all the conditions examined. Isoproterenol- stimulated cyclic adenosine monophosphate (cAMP) accumulation was also increased after 30 minutes (+66%) and 90 minutes (+65%) of insulin injection. Basal and forskolin-stimulated intracellular cAMP values were unchanged. We conclude that, even after a strong release of catecholamines, β-AR redistribution cannot be demonstrated on MNLs.

Original languageEnglish
Pages (from-to)197-201
Number of pages5
JournalThe Journal of Laboratory and Clinical Medicine
Volume119
Issue number2
Publication statusPublished - 1992

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Hypoglycemic Agents
Adrenergic Receptors
Catecholamines
Insulin
Mononuclear Leukocytes
Cyclic AMP
Epinephrine
Injections
Adrenal Medulla
Colforsin
Isoproterenol
Hypoglycemia
Norepinephrine

ASJC Scopus subject areas

  • Medicine(all)
  • Pathology and Forensic Medicine

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High plasma levels of catecholamines during insulin-induced hypoglycemic stress do not cause β-adrenergic receptor sequestration. / Negri, F.; Fratelli, M.; Fratino, P.; D'Eril, G. M.; Finardi, G.; De Blasi, A.

In: The Journal of Laboratory and Clinical Medicine, Vol. 119, No. 2, 1992, p. 197-201.

Research output: Contribution to journalArticle

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AU - Finardi, G.

AU - De Blasi, A.

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AB - In the present investigation insulin-induced hypoglycemia was used as a powerful stimulus to rapidly release epinephrine from the adrenal medulla. Insulin injection raised epinephrine 16-fold and doubled norepinephrine plasma levels. The aim of this attempt was to induce β-adrenergic receptors (β-ARs) sequestration in vivo on mononuclear leukocytes (MNLs). The number of total and surface β-ARs was significantly increased 30 minutes after insulin administration, with only partial recovery at 90 minutes. No detectable receptor sequestration was observed: surface receptors were about 90% of total receptors in all the conditions examined. Isoproterenol- stimulated cyclic adenosine monophosphate (cAMP) accumulation was also increased after 30 minutes (+66%) and 90 minutes (+65%) of insulin injection. Basal and forskolin-stimulated intracellular cAMP values were unchanged. We conclude that, even after a strong release of catecholamines, β-AR redistribution cannot be demonstrated on MNLs.

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