Effect of cetirizine on antigen-induced tracheal contraction of passively sensitized guinea pigs

• Published in: Annals of allergy, asthma, & immunology Vol. 77; no. 4; p. 310
• Main Authors: Dobashi, K, Iizuka, K, Houjou, S, Sakai, H, Watanabe, K, Mori, M, Nakazawa, T
• Format: Journal Article
• Language: English
• Published: United States 01.10.1996
• Subjects: Animals; Anti-Allergic Agents - pharmacology; Antigens; Calcium - analysis; Cells, Cultured; Cetirizine - pharmacology; Guinea Pigs; Histamine - immunology; Histamine - pharmacology; Histamine H1 Antagonists - pharmacology; Histamine Release; In Vitro Techniques; Lung - metabolism; Male; Mast Cells - chemistry; Mice; Mice, Inbred BALB C; Muscle Contraction - drug effects; Pyrilamine - pharmacology; Trachea - physiology
• ISSN: 1081-1206
• DOI: 10.1016/S1081-1206(10)63326-1

Cetirizine dihydrochloride (cetirizine), a potent histamine H1-receptor antagonist, has been developed as an anti-allergy drug. The anti-allergic effects and mechanism of cetirizine were studied using in vitro assay systems. We investigated the effect of cetirizine on antigen-induced contractions of isolated tracheal strips and on chemical mediator release from antigen-stimulated lung chips taken from passively sensitized guinea pigs. We examined the antigen-induced mobilization of Ca2+ in MC/9 mast cells sensitized with IgE. Cetirizine inhibited the antigen-induced contraction of isolated guinea-pig trachea concentration dependently. Pyrilamine, another histamine H1-receptor antagonist, delayed the response but did not change the maximum amplitude. Cetirizine at the concentration of 3 microM also inhibited the antigen-induced release of histamine, leukotriene D4, and leukotriene E4 from guinea pig lung chips. Furthermore, it inhibited the antigen-induced Ca2+ increase in MC/9 mast cells, whereas pyrilamine did not. These findings suggest that one anti-allergic mechanism of cetirizine may inhibit mediator release which is, at least partially, mediated by a decrease in the transient Ca2+ influx in mast cells.