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

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 [Formula: see text] levels over vehicle. Addition of NE to interleukin-1β (IL-1β) significantly increased inducible NO synthase (iNOS) mRNA expression, iNOS protein, and [Formula: see text] production vs. IL-1β alone. Addition of the α-adrenergic blocker prazosin or the β-adrenergic blocker propranolol partially reduced the NE-mediated increase in iNOS mRNA expression and[Formula: see text] production. Addition of prazosin and propranolol together completely abolished the NE-induced increase in iNOS mRNA expression and[Formula: see text] 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 [Formula: see text]production. We report for the first time that NE enhances IL-1β-stimulated NO production by activation of α- and β-adrenergic receptors through a novel MAP kinase mechanism.