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1 Second Department of Internal Medicine and 2 Department of Laboratory Sciences, Gunma University School of Medicine, Maebashi 371, Japan
To determine whether
ANG II as well as mechanical stress affect the production of tumor
necrosis factor (TNF) in the heart, neonatal rat cardiac myocytes and
fibroblasts were cultured separately and treated for 6 h with ANG II,
lipopolysaccharide (LPS), or cyclic mechanical stretch. LPS induced the
production of TNF in cardiac myocytes and fibroblasts. However, TNF
synthesis in fibroblasts was 20- to 40-fold higher than in myocytes.
ANG II (
10
8 M) and
mechanical stretch stimulated the production of TNF in cardiac
fibroblasts but not in myocytes. Furthermore, both ANG II and LPS
increased the expression of TNF-
mRNA in cardiac fibroblasts. Isoproterenol inhibited both LPS- and ANG II-induced production of TNF
in cardiac fibroblasts with increasing intracellular cAMP level.
Moreover, both isoproterenol and dibutyryl cAMP inhibited LPS-induced
TNF- mRNA expression. Thus activation of the renin-angiotensin system, as well as mechanical stress, can stimulate production of TNF
in cardiac fibroblasts. Furthermore, 
-adrenergic receptors may be
responsible for the regulation of TNF synthesis at the transcriptional
level by elevating intracellular cAMP.
myocyte; rat; isoproterenol; adenosine 3',5'-cyclic monophosphate
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