Amitraz‐induced delay of gastrointestinal transit in mice: Mediated by α2‐adrenergic receptors
Amitraz‐induced delay of gastrointestinal transit in mice: Mediated by α2‐adrenergic receptors
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双甲脒诱导小鼠胃肠道转运延迟：由α2肾上腺素能受体介导
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
Zheng‐Xing Lu
中科院分区：
文献类型：
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作者：
W. Hsu;Zheng‐Xing Lu
皮下注射双甲脒（0.3-3.0 mg/kg）可使清醒小鼠的胃肠道转运出现剂量依赖性延迟。双甲脒的这种作用可被α2-肾上腺素能阻滞剂拮抗，例如，育亨宾哌洛生妥拉唑啉其他无α2阻滞活性的肾上腺素能拮抗剂（胸腺嘧啶、哌唑嗪、酚苄明和普萘洛尔）在研究剂量下未降低双甲脒对胃肠道转运的抑制作用。此外，多巴胺能拮抗剂（氟哌啶醇）、多巴胺能拮抗剂（麦角新碱）、组胺H1-拮抗剂（氯苯那敏）、组胺H2-拮抗剂（西咪替丁）、胆碱能拮抗剂（阿托品和六甲双铵）、GABA能拮抗剂（荷包牡丹碱）和阿片类拮抗剂（纳洛酮）均未改变双甲脒的这种作用。用6-羟基多巴胺预处理小鼠未能拮抗双甲脒的作用。这些结果表明，双甲脒诱导的胃肠道转运延迟由连接后α2-肾上腺素能受体介导，似乎不涉及β-肾上腺素能、多巴胺能、多巴胺能、组胺能、胆碱能、GABA能或阿片受体的激活。
Subcutaneous injection of amitraz (0.3–3.0 mg/kg) produced a dose‐dependent delay of gastrointestinal transit in conscious mice. This effect of amitraz was antagonized by α2‐adrenergic blocking agents, e.g., yohimbine, piperoxan, and tolazoline. Other adrenergic antagonists without α2‐blocking activity (thymoxamine, prazosin, phenoxybenzamine, and propranolol) did not reduce the depressant effect of amitraz on gastrointestinal transit at the dosages studied. Furthermore, this effect of amitraz was not altered by a dopaminergic antagonist (haloperidol), a serotonergic antagonist (methysergide), a histamine H1‐antagonist (chlorpheniramine), a histamine H2‐antagonist (cimetidine), cholinergic antagonists (atropine and hexamethonium), a GABAergic antagonist (bicuculline), and an opioid antagonist (naloxone). Pretreatment of mice with 6‐hydroxydopamine failed to antagonize the effect of amitraz. These results suggest that amitraz‐induced delay of gastrointestinal transit is mediated by postjunctional α2‐adrenergic receptors and appears not to involve the activation of β‐adrenergic, dopaminergic, serotonergic, histaminergic, cholinergic, GABAergic, or opioid receptors.