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Vol. 288, Issue 3, 1349-1356, March 1999
Department of Pharmacology and Experimental Therapeutics, Tufts
University School of Medicine, Boston, Massachusetts
Urocortin (Ucn) is related to corticotropin-releasing hormone (CRH),
and both are released in the brain under stress where they stimulate
CRH 1 and 2 receptors (CRHR). Outside the brain, they may have
proinflammatory actions through activation of mast cells, which are
located perivascularly close to nerve endings and degranulate in
response to acute psychological stress. Here, we report that a
concentration of intradermal Ucn as low as 10 nM induced dose-dependent
rat skin mast cell degranulation and increased vascular permeability.
This effect appeared to be equipotent to that of calcitonin
gene-related peptide and neurotensin. Ucn-induced skin vasodilation was
inhibited by pretreatment with the mast cell stabilizer disodium
cromoglycate (cromolyn) and was absent in the mast cell-deficient
W/Wv mice. The selective nonpeptide CRH receptor 1 antagonist, antalarmin and the nonselective peptide antagonist
astressin both reduced vascular permeability triggered by Ucn but not
that by Substance P or histamine. In contrast, the peptide antagonist
-helical CRH-(9-41) reduced the effect of all three. The
vasodilatory effect of Ucn was largely inhibited by pretreatment with
H1 receptor antagonists, suggesting that histamine is the
major mediator involved in vitro. Neuropeptide depletion of sensory
neurons, treatment with the ganglionic blocker hexamethonium, or in
situ skin infiltration with the local anesthetic lidocaine did not
affect Ucn-induced vascular permeability, indicating that its in situ
effect was not mediated through the peripheral nervous system. These
results indicate that Ucn is one of the most potent triggers of rat
mast cell degranulation and skin vascular permeability. This effect of
Ucn may explain stress-induced disorders, such as atopic dermatitis or
psoriasis, and may lead to new forms of treatment.
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