作者: Justus Benrath , Christoph Eschenfelder , Manfred Zimmermann , Frank Gillardon
DOI: 10.1016/0926-6917(95)90022-5
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摘要: Evidence from our previous work suggests that neurogenic mediators contribute to the inflammation following ultraviolet (UV) irradiation of skin. We have investigated whether calcitonin gene-related peptide (CGRP), substance P and nitric oxide (NO) participate in cutaneous inflammatory reaction rat hind paw ear UV irradiation. Skin blood flow was measured by laser Doppler technique. Oedema quantified using a spring loaded micrometer measure thickness. skin lead long lasting increase flow. This dose dependently attenuated CGRP receptor antagonist CGRP-(8-37) (0.15 nmol 25 microliters 6.0 microliters, s.c.) up 51% with maximum effectiveness at 24 h post The inhibitor NO synthase NG-nitro-L-arginine methyl ester hydrochloride (L-NAME, 38%. Concurrent injections s.c. (1.5 12.5 microliters) L-NAME (25 demonstrated an augmentive effect attenuating tachykinin NK1 CP-96,345 (6.0 27%. NG-Nitro-D-arginine (D-NAME) CP-96.344 showed no effects on after (0.6 10 i.d. (10 had oedema formation Furthermore, enhanced CGRP- synthase-immunoreactivity nerve fibres exposed area were visible. Taken these findings together we suggest involvement neuropeptides neuronal vasodilatory component UV-induced contributing vasodilation acts endothelial NO-independent manner.