Histamine-induced vasodilations mediated by H1- and H2-receptors in isolated rat common carotid arteries
Histamine-induced vasodilations mediated by H1- and H2-receptors in isolated rat common carotid arteries
复制标题
离体大鼠颈总动脉中 H1 和 H2 受体介导的组胺诱导血管舒张
DOI：
10.1007/bf02125095
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发表时间：
2005
影响因子：
1.5
通讯作者：
M. Tsukada
中科院分区：
文献类型：
--
作者：
S. Chiba;M. Tsukada
摘要使用插管插入方法，在分离的、灌注的大鼠颈总动脉制剂中使用选择性组胺 H1 和 H2 受体激动剂和拮抗剂，分析组胺的血管舒张作用，该制剂通过连续输注去氧肾上腺素和普萘洛尔进行预收缩。组胺、2-吡啶乙胺 (2-PEA)（一种选择性 H1 激动剂）和 dimaprit（一种选择性 H2 激动剂）以剂量相关的方式产生血管舒张作用。效力顺序为组胺>dimaprit>2-PEA。苯海拉明（一种选择性 H1 拮抗剂）或西咪替丁（一种选择性 H2 拮抗剂）可显着抑制组胺诱导的扩张。苯海拉明显着抑制 2-PEA 诱导的扩张，但西咪替丁则不显着抑制。西咪替丁可显着阻断地马普利引起的扩张，但苯海拉明则不能。内皮细胞的去除显着抑制了 ACh、组胺、2-PEA 和 dimaprit 诱导的扩张。从这些结果可以得出以下结论：(1) 离体大鼠颈总动脉同时具有 H1- 和 H2- 受体，(2) 血管收缩性 H1- 受体很少，(3) H1- 和 H2- 受体仅介导血管舒张而不介导血管收缩，(4) 来自内皮的 EDRF 可能不仅通过 H1- 还通过 H1- 参与组胺诱导的血管舒张。 H2-受体。
SummaryUsing the cannula inserting method, the vasodilatory effects of histamine were analysed employing selective histamine H1- and H2-receptor agonists and antagonists in isolated, perfused rat common carotid arterial preparations which were preconstricted by a continuous infusion of phenylephrine with propranolol. Histamine, 2-pyridylethylamine (2-PEA) (a selective H1-agonist) and dimaprit (a selective H2-agonist) produced a vasodilation in a dose-related manner. The order of potency was histamine > dimaprit > 2-PEA. Histamine-induced dilations were significantly inhibited by either diphenhydramine (a selective H1-antagonist) or cimetidine (a selective H2-antagonist). 2-PEA-induced dilations were significantly inhibited by diphenhydramine but not by cimetidine. Dimaprit-induced dilations were significantly blocked by cimetidine but not by diphenhydramine. ACh-, histamine-, 2-PEA- and dimaprit-induced dilations were significantly suppressed by removal of the endothelium. From these results, it is concluded that (1) isolated rat common carotid arteries have both H1-and H2-receptors, (2) there are few vasoconstrictory H1-receptors, (3) both H1- and H2-receptors mediate only vasodilation but not vasoconstriction, and (4) EDRF from the endothelium might participate in histamine-induced vasodilation via not only H1- but also H2-receptors.