Norepinephrine inhibits energy metabolism of human peripheral blood mononuclear cells via adrenergic receptors

• Published in: Bioscience reports Vol. 21; no. 5; pp. 627 - 635
• Main Authors: Lünemann, J D, Buttgereit, F, Tripmacher, R, Baerwald, C G, Burmester, G R, Krause, A
• Format: Journal Article
• Language: English
• Published: England 01.10.2001
• Subjects: Adrenergic alpha-Antagonists - pharmacology; Adrenergic beta-Antagonists - pharmacology; Energy Metabolism - drug effects; Humans; Monocytes - drug effects; Monocytes - metabolism; Norepinephrine - pharmacology; Oxygen Consumption - drug effects; Phentolamine - pharmacology; Propranolol - pharmacology; Receptors, Adrenergic - metabolism
• ISSN: 0144-8463; 1573-4935
• DOI: 10.1023/A:1014768909442

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.