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Am J Physiol Heart Circ Physiol 276: H47-H52, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 1, H47-H52, January 1999

Norepinephrine-stimulated MAP kinase activity enhances cytokine-induced NO production by rat cardiac myocytes

Hong Kan1, Zirong Xie1, and Mitchell S. Finkel1,2,3

Departments of 1 Medicine and 2 Pharmacology, West Virginia University School of Medicine, Robert C. Byrd Health Sciences Center, and 3 Louis A. Johnson Veterans Administration Medical Center, Morgantown, West Virginia 26506-9157

The effect of norepinephrine (NE) on cytokine-stimulated nitric oxide (NO) production by cardiac myocytes has not been previously reported. NE alone caused no significant increase in NO-2 levels over vehicle. Addition of NE to interleukin-1beta (IL-1beta ) significantly increased inducible NO synthase (iNOS) mRNA expression, iNOS protein, and NO-2 production vs. IL-1beta alone. Addition of the alpha -adrenergic blocker prazosin or the beta -adrenergic blocker propranolol partially reduced the NE-mediated increase in iNOS mRNA expression and NO-2 production. Addition of prazosin and propranolol together completely abolished the NE-induced increase in iNOS mRNA expression and NO-2 production. NE significantly enhanced mitogen-activated protein (MAP) kinase activity that was reduced by prazosin, propranolol, and PD-98059, a selective MAP kinase kinase inhibitor. Addition of PD-98059 reduced the NE-mediated increase in iNOS mRNA expression and NO-2 production. We report for the first time that NE enhances IL-1beta -stimulated NO production by activation of alpha - and beta -adrenergic receptors through a novel MAP kinase mechanism.

interleukin-1beta ; adrenergic receptors; protein kinases; cell signaling


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