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Inflammatory oedema induced by synergism between calcitonin gene‐related peptide (CGRP) and mediators of increased vascular permeability
Author(s) -
Brain S.D.,
Williams T.J.
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb11107.x
Subject(s) - calcitonin gene related peptide , bradykinin , substance p , endocrinology , chemistry , medicine , histamine , neurokinin a , vasodilation , calcitonin , vascular permeability , prostaglandin , neuropeptide , pharmacology , receptor
1 The potent vasodilator calcitonin gene‐related peptide (CGRP, human synthetic), when mixed with histamine and injected intradermally in the rabbit, induced a marked potentiation of local oedema. 2 CGRP also potentiated oedema induced by other mediators of increased microvascular permeability in the rabbit; bradykinin, platelet‐activating factor (Paf), C5a des Arg, N ‐formylmethionyl‐leucyl‐phenylalanine (FMLP) and leukotriene B 4 (LTB 4 ). 3 Substance P alone, or mixtures of substance P and CGRP, failed to induce oedema in rabbit skin. In rat skin, however, substance P induced oedema and this was potentiated by CGRP. 4 CGRP had a protracted potentiating action following intradermal injection in the rabbit. The time for half loss of activity for CGRP was 40.1 ± 7.5 min compared to 18 ± 1 min for prostaglandin E 2 (PGE 2 ). 5 No loss of potentiating activity was detected after incubation of CGRP in rabbit plasma or blood for 60 min. 6 We postulate that endogenous CGRP, if released locally from nerve endings, could have a marked enhancing effect on oedema induced by other mediators in an inflammatory reaction.