Yamasaki Y, Shimamura O, Kizu A, Nakagawa M, Ijichi H
Agents Actions. 1983 Jun;13(4):310-7. doi: 10.1007/BF01971482.
The formaldehyde method was used to examine the effects of clonidine and methoxamine on IgE-mediated 14C-serotonin release from rat mast cells in vitro. Clonidine (10(-11) -10(-8) M) caused dose-related enhancement of the mediator release 7 min after the antigen challenge; yohimbine (10(-6) M) blocked this enhancement by clonidine (10(-6) M), but prazosin (10(-6) M) did not. Methoxamine did not enhance this immunological release reaction at concentrations up to 10(-6) M. PGE1 (2 X 10(-8) -2 X 10(-5) M), isoproterenol (10(-10) -10(-8) M), dopamine (4 X 10(-8) -4 X 10(-8) M) and aminophylline (6 X 10(-6) -6 X 10(-4) M) caused dose-related inhibition of this mediator release 1 min after antigen challenge. Clonidine (10(-13) -10(-12) M), but not methoxamine (10(-8) -10(-6) M), reversed dose-dependently this inhibition of mast cells by PGE1 (2 X 10(-6) M), isoproterenol (10(-8) M), dopamine (4 X 10(-6) M); yohimbine (10(-8) M) antagonized this reversing action of clonidine (10(-12) M), but prazosin (10(-10) M) did not. Neither clonidine (10(-14) -10(-11) M) nor methoxamine (10(-8) -10(-6) M) reversed the inhibitory action of aminophylline (2 X 10(-4) M). These results suggests that clonidine enhances IgE-mediated 14C-serotonin release from rat mast cells and also antagonizes the inhibition of mast cells by PGE1, isoproterenol and dopamine, but not by aminophylline in this immunological reaction through alpha 2-adrenergic receptors, and that the inhibition of adenylate cyclase of mast cells is one of the biochemical actions of alpha 2-adrenergic mechanisms.
采用甲醛法体外检测可乐定和甲氧明对大鼠肥大细胞IgE介导的14C - 5 -羟色胺释放的影响。抗原激发后7分钟，可乐定（10(-11) - 10(-8) M）引起介质释放呈剂量依赖性增强；育亨宾（10(-6) M）可阻断可乐定（10(-6) M）引起的这种增强作用，但哌唑嗪（10(-6) M）则不能。在浓度高达10(-6) M时，甲氧明未增强这种免疫释放反应。抗原激发后1分钟，前列腺素E1（2×10(-8) - 2×10(-5) M）、异丙肾上腺素（10(-10) - 10(-8) M）、多巴胺（4×10(-8) - 4×10(-8) M）和氨茶碱（6×10(-6) - 6×10(-4) M）引起介质释放呈剂量依赖性抑制。可乐定（10(-13) - 10(-12) M）可剂量依赖性地逆转前列腺素E1（2×10(-6) M）、异丙肾上腺素（10(-8) M）、多巴胺（4×10(-6) M）对肥大细胞的这种抑制作用，但甲氧明（10(-8) - 10(-6) M）则不能；育亨宾（10(-8) M）可拮抗可乐定（10(-12) M）的这种逆转作用，但哌唑嗪（10(-10) M）则不能。可乐定（10(-14) - 10(-11) M）和甲氧明（10(-8) - 10(-6) M）均不能逆转氨茶碱（2×10(-4) M）的抑制作用。这些结果表明，可乐定可增强大鼠肥大细胞IgE介导的14C - 5 -羟色胺释放，并拮抗前列腺素E1、异丙肾上腺素和多巴胺对肥大细胞的抑制作用，但在该免疫反应中不拮抗氨茶碱的作用，其作用是通过α2 -肾上腺素能受体实现的，且肥大细胞腺苷酸环化酶的抑制是α2 -肾上腺素能机制的生化作用之一。
