Quantitation of phototoxic hyperemia and permeability to protein: II. Inhibition by histamine (H1 and H2) receptor antagonists in mouse skin.
Exposure of anthracene treated skin to long-wave ultraviolet radiation (UVA) will produce hyperemia, increased vascular permeability, burning and itching. This photosensitized inflammation was produced in the skin of hairless mice by the topical application of a 0.025% (w/v) solution of anthracene followed by exposure to UVA. The resultant hyperemia was quantified by the increase in 51Cr-erythrocyte content (cpm/wet weight) of skin. After 1000 sec (1.3 x 10(4)J/ M2) of UVA, the blood content of the skin had increased nine-fold. Pyrilamine (H1 antagonist), administered orally, did not inhibit the hyperemia in response to anthracene-UVA, whereas cimetidine (H2 antagonist) increased the blood content of the skin. However, a combination of pyrilamine and cimetidine significantly inhibited the hyperemia, indicating that histamine may mediate the anthracene-UVA hyperemia via H1 and H2 receptors on dermal vessels. Since neither antagonist alone blocked the response, the mechanism of histamine action in this response may involve histamine receptors on other dermal components in addition to the blood vessels. In particular, the exacerbation of this photosensitized inflammation by cimetidine lends support to the concept of H2 receptors on mast cells which negatively modulate histamine release.[1]References
- Quantitation of phototoxic hyperemia and permeability to protein: II. Inhibition by histamine (H1 and H2) receptor antagonists in mouse skin. Argenbright, L.W., Forbes, P.D., Stewart, G.J. J. Invest. Dermatol. (1980) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
