作者: J Szelényi , J.P Kiss , E.S Vizi
DOI: 10.1016/S0165-5728(99)00234-9
关键词: In vivo 、 Endocrinology 、 Internal medicine 、 Sympathetic nervous system 、 Receptor 、 Medicine 、 Adrenergic 、 Cytokine 、 Tumor necrosis factor alpha 、 Lipopolysaccharide 、 Reserpine
摘要: Abstract In the present study, regulation of tumor necrosis factor-α (TNF-α) production by α2- and β-adrenoceptors located on noradrenergic nerve terminals macrophages was studied in endotoxaemic mice. We found that reduction sympathetic outflow reserpine dramatically increased lipopolysaccharide (LPS)-induced TNF-α production, demonstrating release endogenous noradrenaline (NA), controlled presynaptic α2-adrenoceptors, a determinant factor this model. By using β-adrenergic drugs (clonidine, CH-38083, isoproterenol, propranolol) we provided first vivo evidence that, beside dominance neuronal macrophage β-adrenoceptors, α2-adrenoceptors were also involved modulation LPS-induced production. Since adrenergic are widely used clinical practice, our findings may have therapeutical implications.