Aconitine induces bradycardia through a transmission pathway including the anterior hypothalamus in conscious mice.

Abstract:

:Aconitine administered intraperitoneally (i.p.) produces bradycardia mainly by a central muscarinic action. The involvement of hypothalamic regions in the occurrence of aconitine-induced bradycardia was investigated in hypothalamus-lesioned mice. The lesions were made by passing a direct current (1.5 mA, 13 s) through a monopolar electrode. The aconitine (30 micrograms/kg, i.p.)-induced bradycardia was prevented by bilateral lesions of either the whole hypothalamus, except for the lateral hypothalamus area, or the anterior hypothalamus (AH). The bradycardia was not prevented by bilateral lesions of the ventromedial, the paraventricular, the posterior or the lateral hypothalamus regions. Bupivacaine, but not atropine (1 microgram, administered into the intact AH) prevented aconitine-induced bradycardia in mice with a contralaterally lesioned AH. Aconitine (0.8 microgram) directly administered into the unilateral AH in intact mice caused a late phase and lesser extent of bradycardia. These results suggest that a transmission pathway including the AH contributes to the aconitine-induced bradycardia but does not involve the activation of muscarinic receptors in the AH.

journal_name

Biol Pharm Bull

authors

Kimura I,Takada M,Nojima H

doi

10.1248/bpb.20.856

subject

Has Abstract

pub_date

1997-08-01 00:00:00

pages

856-60

issue

8

eissn

0918-6158

issn

1347-5215

journal_volume

20

pub_type

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