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Mast cells are involved in atopic disorders, often exacerbated by stress, and are located perivascularly close to sympathetic and sen- sory nerve endings. Mast cells are activated by electrical nerve stim- ulation and millimolar concentrations of neuropeptides, such as sub- stance P (SP). Moreover, acute psychological stress induces CRH- dependent mast cell degranulation. Intradermal administration of rat/human CRH (0.1-10 mM) in the rat induced mast cell degranu- lation and increased capillary permeability in a dose-dependent fash- ion. The effect of CRH on Evans blue extravasation was stronger than equimolar concentrations of the mast cell secretagogue compound 48/80 or SP. The free acid analog of CRH, which does not interact with its receptors (CRHR), had no biological activity. Moreover, systemic administration of antalarmin, a nonpeptide CRHR1 antagonist, pre- vented vascular permeability only by CRH and not by compound 48/80 or SP. CRHR1 was also identified in cultured leukemic human mast cells using RT-PCR. The stimulatory effect of CRH, like that of com- pound 48/80 on skin vasodilation, could not be elicited in the mast cell deficient W/Wv mice but was present in their 1/1 controls, as well as in C57BL/6J mice; histamine could still induce vasodilation in the W/Wv mice. Treatment of rats neonatally with capsaicin had no effect on either Evans blue extravasation or mast cell degranulation, indi- cating that the effect of exogenous CRH in the skin was not secondary to or dependent on the release of neuropeptides from sensory nerve endings. The effect of CRH on Evans blue extravasation and mast cell degranulation was inhibited by the mast cell stabilizer disodium cromoglycate (cromolyn), but not by the antisecretory molecule so- matostatin. To investigate which vasodilatory molecules might be involved in the increase in vascular permeability, the CRH injection site was pretreated with the H1-receptor antagonist diphenhydra- mine, which largely inhibited the CRH effect, suggesting that hista- mine was involved in the CRH-induced vasodilation. The possibility that nitric oxide might also be involved was tested using pretreatment with a nitric oxide synthase inhibitor that, however, increased the effect of CRH. These findings indicate that CRH activates skin mast cells at least via a CRHR1-dependent mechanism leading to vasodi- lation and increased vascular permeability. The present results have implications for the pathophysiology and possible therapy of skin disorders, such as atopic dermatitis, eczema, psoriasis, and urticaria, which are exacerbated or precipitated by stress. (Endocrinology 139: 403- 413, 1998)

endocrinology

Corticotropin-Releasing Hormone Induces Skin Mast Cell Degranulation and Increased Vascular Permeability, A Possible Explanation for Its Proinflammatory Effects