Catecholamines stimulate interleukin-6 synthesis in rat cardiac fibroblasts

Carl-Ludwig-Institut für Physiologie, Universität Leipzig, D-04103 Leipzig, Germany Proinflammatory cytokines have been implicated in the pathophysiology of different heart diseases. Recent evidence suggests that interleukin-6 (IL-6) may play a role in mechanisms leading to cardiac hypertrophy. In a...

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Published in:American journal of physiology. Heart and circulatory physiology 2001-07, Vol.281 (1), p.H14-H21
Main Authors: Burger, Antje, Benicke, Markus, Deten, Alexander, Zimmer, Heinz-Gerd
Format: Article
Language:English
Subjects:
Animals
Cells, Cultured
Cytokines - genetics
Female
Fibroblasts - drug effects
Fibroblasts - metabolism
Fibroblasts - physiology
Gene Expression - drug effects
Interleukin-6 - biosynthesis
Interleukin-6 - genetics
Myocardium - cytology
Myocardium - metabolism
Norepinephrine - pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, alpha - physiology
Receptors, Adrenergic, beta - physiology
RNA, Messenger - metabolism
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Summary:Carl-Ludwig-Institut für Physiologie, Universität Leipzig, D-04103 Leipzig, Germany Proinflammatory cytokines have been implicated in the pathophysiology of different heart diseases. Recent evidence suggests that interleukin-6 (IL-6) may play a role in mechanisms leading to cardiac hypertrophy. In addition, catecholamines are known to induce cardiac hypertrophy. In the present study, we examined whether cardiac fibroblasts may be a potential source of IL-6 production in the rat heart and whether catecholamines can modulate the IL-6 synthesis. Only a small amount of IL-6 mRNA was detected in unstimulated rat cardiac fibroblasts. However, a 50-fold increase of IL-6 mRNA was found after stimulation with norepinephrine (NE). Addition of carvedilol, a - and -adrenergic receptor antagonist, prevented almost completely the NE-induced synthesis of IL-6 mRNA. Phenylephrine, an -adrenergic agonist, and isoproterenol, a -adrenergic agonist, also induced an increase in IL-6. However, the stimulation via -receptors led to a more pronounced elevation. These data show that NE increases IL-6 expression in rat cardiac fibroblasts and that IL-6 may play an important autocrine/paracrine role in cardiac disease states associated with hypertrophy. cytokines; norepinephrine; cardiac hypertrophy; adrenergic receptor blocker
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2001.281.1.h14