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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Modulatory action of potassium channel openers on field potential and histamine release from rat peritoneal mast cells.
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Modulatory action of potassium channel openers on field potential and histamine release from rat peritoneal mast cells.

机译：钾通道开放剂对大鼠腹膜肥大细胞场电位和组胺释放的调节作用。

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摘要

To determine whether changes in membrane potential affect the extent of mast cell degranulation, compound 48/80 was added to rat peritoneal mast cell suspensions in the absence or presence of potassium channel openers (KCOs). Changes were compared between the field potential (FP) and the amount of histamine released. The results demonstrated that (i) the onset and duration of FP, which reflects the hyperpolarizing nature of the response, increased as the concentration of compound 48/80 increased; (ii) both FP and the amount of histamine released increased as the concentration of compound 48/80 increased; (iii) although both KCOs (SDZ PCO400, a benzopyran derivative, and P1060, a cyanoguanidine derivative) potentiated compound 48/80-induced increases in FP and histamine release, without compound 48/80, they had no effect on either parameter; (iv) both glibenclamide and charybdotoxin significantly attenuated the compound 48/80-induced increase in FP; and (v) glibenclamide was able to attenuate the KCO-induced potentiation of FP. The results show that drugs presumably causing hyperpolarization can affect histamine release from rat peritoneal mast cells. The effect of KCOs on compound 48/80-induced response appears to be potentiation in nature rather than synergism. It is possible that KCO hyperpolarizes the cell membrane, enhances Ca2+ influx, and thus increases histamine release. As such, selective blockers of K+ channels may be useful for the treatment of immunological disorders.
机译：为了确定膜电位的变化是否影响肥大细胞脱粒的程度，在不存在或存在钾通道开放剂（KCO）的情况下，将化合物48/80添加至大鼠腹膜肥大细胞悬浮液中。比较场电势（FP）和组胺释放量之间的变化。结果表明：（i）FP的发作和持续时间随着化合物48/80浓度的增加而增加，反映了反应的超极化性质。 （ii）FP和组胺的释放量均随着化合物48/80浓度的增加而增加; （iii）尽管两种KCO（SDZ PCO400，苯并吡喃衍生物和P1060，氰基胍衍生物）都增强了化合物48/80诱导的FP和组胺释放的增加，但没有化合物48/80，它们对这两个参数均没有影响; （iv）格列本脲和炭疽毒素均显着减弱了化合物48/80引起的FP升高; （v）格列本脲能够减弱KCO诱导的FP增强作用。结果表明，可能引起超极化的药物可以影响组胺从大鼠腹膜肥大细胞的释放。 KCO对化合物48/80诱导的反应的作用似乎是自然增强而不是协同作用。 KCO有可能使细胞膜超极化，增强Ca2 +流入，从而增加组胺的释放。这样，K +通道的选择性阻滞剂可用于治疗免疫学疾病。

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