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Amitraz‐induced delay of gastrointestinal transit in mice: Mediated by α 2 ‐adrenergic receptors
Author(s) -
Hsu Walter H.,
Lu ZhengXing
Publication year - 1984
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430040608
Subject(s) - histaminergic , yohimbine , pharmacology , methysergide , antagonist , phenoxybenzamine , tolazoline , hexamethonium , endocrinology , (+) naloxone , prazosin , chemistry , reserpine , medicine , adrenergic antagonist , histamine , atropine , receptor , propranolol
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 α 2 ‐adrenergic blocking agents, e.g., yohimbine, piperoxan, and tolazoline. Other adrenergic antagonists without α 2 ‐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 H 1 ‐antagonist (chlorpheniramine), a histamine H 2 ‐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 α 2 ‐adrenergic receptors and appears not to involve the activation of β‐adrenergic, dopaminergic, serotonergic, histaminergic, cholinergic, GABAergic, or opioid receptors.