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Am J Physiol Heart Circ Physiol 276: H141-H148, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 1, H141-H148, January 1999

Suppression of beta -adrenergic responsiveness of L-type Ca2+ current by IL-1beta in rat ventricular myocytes

Shi J. Liu1,2, Weiguo Zhou3, and Richard H. Kennedy2

Departments of 1 Biopharmaceutical Sciences, 2 Pharmacology and Toxicology, and 3 Anesthesiology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205

The possible mechanism by which interleukin-1beta (IL-1beta ) affects beta -adrenergic responsiveness of L-type Ca2+ current (ICa,L) was examined in adult rat ventricular myocytes by use of whole cell patch-clamp techniques. In the presence of isoproterenol (Iso), exposure for 3 min to IL-1beta suppressed the Iso-activated ICa,L. In the presence of IL-1beta , the response of ICa,L to Iso was decreased, and the EC50 for Iso stimulation was increased. However, IL-1beta had no effect on [3H]CGP-12177 binding, displacement of [3H]CGP-12177 binding by Iso, or on basal and Iso-enhanced cAMP content. When ICa,L was activated by extracellular application of forskolin or 8-(4-chlorophenylthio)-cAMP, a membrane-permeable cAMP analog, or by intracellular dialysis with cAMP, IL-1beta had little effect on ICa,L. In contrast, in the presence of cAMP, IL-1beta still suppressed the Iso-enhanced ICa,L. These results show that the IL-1beta -induced decrease in beta -adrenergic responsiveness of ICa,L does not result from inhibition of beta -adrenoceptor binding, adenylyl cyclase activity, or cAMP-mediated pathways, suggesting a cAMP-independent mechanism.

cytokines; calcium channel; signal transduction; cardiac myocytes


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