Sakuta H
Department of Pharmacology, National Defense Medical College, Saitama, Japan.
Eur J Pharmacol. 1994 Jan 1;266(1):99-102. doi: 10.1016/0922-4106(94)90214-3.
Effects of histamine receptor ligands on the glibenclamide-sensitive K+ currents induced by K+ channel openers, cromakalim and Y-26763, were examined in follicle-enclosed Xenopus oocytes. Histamine H1 receptor antagonists, promethazine, dimethindene and chlorpheniramine all decreased cromakalim-induced K+ currents with IC50 values of 31.5 microM, 29.5 microM and 138 microM, respectively. These compounds also blocked Y-26763-induced K+ currents with comparable IC50 values. Histamine (1 mM) and histamine H2 receptor antagonists, cimetidine (0.5 mM) and ranitidine (1 mM) had little effect on these K+ currents. These results suggest that histamine H1 receptor antagonists inhibit glibenclamide-sensitive K+ currents by a mechanism other than the histamine H1 receptor antagonism. The inhibitory effects might explain, in part, the reported actions of histamine H1 receptor antagonists in ischemia.
在卵泡包被的非洲爪蟾卵母细胞中，研究了组胺受体配体对钾通道开放剂（克罗卡林和Y-26763）诱导的格列本脲敏感钾电流的影响。组胺H1受体拮抗剂异丙嗪、二甲茚定和氯苯那敏均降低了克罗卡林诱导的钾电流，IC50值分别为31.5 microM、29.5 microM和138 microM。这些化合物也以相当的IC50值阻断了Y-26763诱导的钾电流。组胺（1 mM）以及组胺H2受体拮抗剂西咪替丁（0.5 mM）和雷尼替丁（1 mM）对这些钾电流几乎没有影响。这些结果表明，组胺H1受体拮抗剂通过组胺H1受体拮抗作用以外的机制抑制格列本脲敏感钾电流。这种抑制作用可能部分解释了组胺H1受体拮抗剂在缺血中的报道作用。
