Possible Participation of Histamine H3-Receptors in the Regulation of Anaphylactic Histamine Release from Isolated Rat Peritoneal Mast Cells

The Japanese Journal of Pharmacology

Takeshi Nabe¹  Kohji Ogawa¹  Shigekatsu Kohno¹  Hideki Yamamura¹  Katsuya Ohata¹  Shintaro Nakao¹ 

[1] Department of Pharmacology, Kyoto Pharmaceutical University

关键词: (R)-α-Methylhistamine;    Thioperamide;    Histamine;    Mast cell;    Compound 48/80;   

DOI  :  10.1254/jjp.66.173

学科分类：药理学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(26)Cited-By(19)Anaphylactic histamine release from isolated rat peritoneal mast cells was concentration-dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 μM and enhanced by a 20- to 30-min treatment with thioperamide (H3-antagonist) at 3 μM with significance, but little affected by mepyramine (H1-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 106 mast cells/ml. At a low concentration of mast cells (104 mast cells/ml), (R)-α-methylhistamine (α-MH), an H3-agonist, at 0.9-90 μM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by α-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration-dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also α-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells.

【 授权许可】

Unknown