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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
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