Abstract
We know that the mast cell or basophil degranulation and the release of chemical mediators such as histamine may play an important role in inducing immediate type allergic reactions.
In this experiment, employing purified rat peritoneal mast cells (RPMC) the degranulation pattern of RPMC and percent release of histamine from RPMC by pharmacologic (compound 48/80, kallikrein or peptidoglycan) or allergic (IgE-anti IgE complex) stimuli were examined. The inhibitory effects of cate-colamine (isoproterenol), an adenylate cyclase stimulator, methylxanthine (IBMX: 3-isobutyl-l-methyl-xanthine), a phosphodiesterase inhibitor and chemical mediators (histamine, serotonin, bradykinin) on compound 48/80-induced RPMC degranulation and also those of catecolamine, methylxanthine and chemical mediators on IgE-anti IgE complex-induced histamine release from RPMC were tested.
Compound 48/80-induced RPMC degranulation was remarkably inhibited not only by treatment with isoproterenol and IBMX, but also by treatment with histamine. It was not, however, inhibited by serotonin or bradykinin. The inhibitory effect of histamine on compound 48/80-induced RPMC degranulation was blocked by pretreatment with H2-antagonist (cimetidine), but not by Hl-antagonist (diphenhydramine). The cyclic adenosine 3', 5'-monophosphate (cAMP) content of RPMC was significantly increased by pretreatment with histamine as well as isoproterenol and IBMX.
These facts suggest that cAMP acts as a regulator or modulator of the RPMC degranulation and the histamine release from mast cells and that the inhibitory effect induced by histamine may be related to the H2-receptor existing on the surface of mast cells.
