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Am J Physiol Regul Integr Comp Physiol 279: R2156-R2163, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 6, R2156-R2163, December 2000

Role of NO and PAF in the impairment of skeletal muscle contractility induced by TNF-alpha

Giuseppe Alloatti1,2, Claudia Penna1, Filippo Mariano3, and Giovanni Camussi3

1 Laboratorio di Fisiologia Generale, Dipartimento di Biologia Animale e dell'Uomo, 2 Istituto Nazionale per la Fisica della Materia and 3 Dipartimento di Medicina Interna, Università degli Studi di Torino, 10123 Torino, Italy

The role of platelet-activating factor (PAF) and nitric oxide (NO) as mediators of the effects of tumor necrosis factor-alpha (TNF-alpha ) on skeletal muscle contractility was studied in guinea pig extensor digitorum longus (EDL) muscle. TNF-alpha (5-10 ng/ml) reduced contractility at every stimulation frequency (1-200 Hz) and shifted the force-frequency relationship to the right. The role of NO and PAF as mediators of TNF-alpha was suggested by the protective effect of NG-nitro-L-arginine methyl ester (L-NAME; 1 mM), but not of NG-nitro-D-arginine methyl ester (D-NAME; 1 mM), and by the inhibitory effect of the PAF-receptor antagonist WEB-2170 (3 µM). TNF-alpha increased the production of PAF and NO. Similar to TNF-alpha , both S-nitroso-N-acetylpenicillamine (0.5-1 µM), an NO-generating compound, and PAF (10-20 nM) reduced EDL contractility. L-NAME, but not D-NAME, blocked the negative effect of PAF. Blockade of phospholipase A2, which is required for PAF synthesis, significantly reduced the effects of TNF-alpha . WEB-2170 inhibited NO synthesis induced by TNF-alpha and PAF-stimulated NO production. These results suggest that both PAF and NO contribute to the development of the mechanical alterations induced by TNF-alpha and that NO production is downstream to the synthesis of PAF.

extensor digitorum longus; nitric oxide; platelet-activating factor; tumor necrosis factor-alpha


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