Abstract:
:Previous studies demonstrated that the adaptive response to stressors and inflammatory signals involves the activation of the autonomous [corrected] nervous system. Catecholamines have been shown to modulate the activity of various immune effector cells directly via membrane adrenergic receptors. Here, we investigated immediate effects of norepinephrine on energy metabolism of immune cells. Norepinephrine inhibits oxygen consumption of human peripheral blood mononuclear cells at concentrations that are relevant to its physiological range. The beta-adrenoreceptor antagonist propranolol, but not the alpha-adrenoreceptor antagonist phentolamine reversed the norepinephrine induced inhibition in quiescent cells. Conversely, phentolamine but not propranolol is capable of blocking norepinephrine mediated effects in mitogen activated human peripheral blood mononuclear cells. Our data indicate that the sensitization of alpha- and beta-adrenoreceptors on immune cells is differentially regulated, and that these processes depend on the activation state of these cells. These findings have important implications for the understanding of stress-induced suppression of immune function and may contribute to the elucidation of the pathogenesis of immunologically mediated diseases.
journal_name
Biosci Repjournal_title
Bioscience reportsauthors
Lünemann JD,Buttgereit F,Tripmacher R,Baerwald CG,Burmester GR,Krause Adoi
10.1023/a:1014768909442keywords:
subject
Has Abstractpub_date
2001-10-01 00:00:00pages
627-35issue
5eissn
0144-8463issn
1573-4935journal_volume
21pub_type
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journal_title:Bioscience reports
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