Tumor necrosis factor-alpha prevents interleukin-1 beta from augmenting capsaicin-induced vasodilatation in the rat skin.
The effect of tumor necrosis factor-alpha (TNF alpha) and tumor necrosis factor-beta (TNF beta) on the capsaicin-induced increase in cutaneous blood flow was investigated in anaesthetized rats. Skin blood flow was measured by laser-Doppler flowmetry. Intraplantar subcutaneous injections of 5-500 pg TNF alpha and 50-5000 pg TNF beta had no effect on local blood flow, whereas 5000 pg TNF alpha induced a transient hyperaemia. However, neither the pretreatment with TNF alpha (5-5000 pg) nor that with TNF beta (50-5000 pg) enhanced the vasodilatator response to intraplantar capsaicin (0.03 micrograms; 0.1 microgram), whereas 50 pg interleukin-1 beta augmented the capsaicin-induced hyperaemia (P < 0.05). This enhancement of the cutaneous hyperaemic response to capsaicin was absent when interleukin-1 beta (50 pg) was co-injected with TNF alpha (500 pg or 5000 pg). The vasodilatation caused by calcitonin gene-related peptide or bradykinin was not altered by 500 pg or 5000 pg TNF alpha. These data indicate that TNFs, in contrast to interleukin-1 beta, do not amplify the hyperaemic response to afferent nerve stimulation with capsaicin but reverse the augmentation mediated by interleukin-1 beta.[1]References
- Tumor necrosis factor-alpha prevents interleukin-1 beta from augmenting capsaicin-induced vasodilatation in the rat skin. Herbert, M.K., Hering, S. Eur. J. Pharmacol. (1995) [Pubmed]
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