Premium
Aconitine‐induced bradycardia, centrally acting muscarinic effects are inhibited peripherally by higenamine in conscious mice
Author(s) -
Kimura Ikuko,
Makino Mitsuhiro,
Matsui Tetsuo,
Takada Miwako,
Kimura Masayasu
Publication year - 1994
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.2650080302
Subject(s) - aconitine , bradycardia , atropine , chronotropic , pharmacology , muscarinic acetylcholine receptor , propranolol , anesthesia , medicine , heart rate , chemistry , receptor , blood pressure
The effects of aconitine, higenamine and coryneine derived from processed aconite, a Sino‐Japanese medicine on pulse rate were examined in unanaesthetized mice. The intraperitoneal (i.p.) administration of the water extract (3 mg/kg) of processed aconite produced a bradycardia, like bigeminy, within 15 min which was prolonged for 30 min. Aconitine (30 μg/kg, i.p.) produced a similar bradycardia. Higenamine induced tachycardia at doses of 30 and 100 μg/kg, i.p. The aconitine‐induced bradycardia was antagonized completely by higenamine (10 μg/kg, i.p.), isoproterenol (1 μg/kg. s.c.), or scopolamine (10 μg/kg. s.c.). The anti‐aconitine effect of higenamine was prevented by propranolol (1 mg/kg, i.p.). Centrally administered aconitine (1 and 3μg) also induced bradycardia. The aconitine (i.c.v.)‐induced bradycardia was prevented by centrally administered atropine (1 μg, i.c.v.). These results demonstrated that aconitine (i.p.)‐induced bradycardia is mainly due to a central muscarinic action. As higenamine has a peripheral β 1 ‐adrenergic action, like isoproterenol, the inhibition by higenamine of aconitine‐induced bradycardia is due to physiological antagonism.