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At least 145 records · Page 8Linked to original sources
PubMed1996

Aconitine, a main component of aconite, increases spontaneous acetylcholine release from the frontal cerebral cortex of freely moving rats.

We investigated whether peripherally administered aconitine increases spontaneous acetylcholine (ACh) release from the frontal cerebral cortex in freely moving rats using in vivo microdialysis, as it relates to aconitine-induced bradycardia estimated by a tail-artery cuff technique in unilateral anterior hypothalamus (AH)-lesion mice. Intraperitoneally administered aconitine significantly increased cortical ACh release within 15 min at 10 and 30 micrograms/kg. The increasing effect disappeared 30 min after the administration of aconitine. Aconitine-induced ACh release was not inhibited by intracerebroventricularly preadministered atropine (1 and 3 micrograms/rat). Atropine (1 micrograms/mouse) preadministered into the contralateral intact AH in mice did not affect aconitine (30 micrograms/kg, i.p.)-induced bradycardia. These results indicate that the cortical ACh release caused by peripherally administered aconitine does not occur through activation of the central muscarine receptor, and thus its ACh release may not be concerned with the occurrence of bradycardia.

Acetylcholine↗
PubMed1999

Inhibition of activation of nuclear factor kappaB is responsible for inhibition of inducible nitric oxide synthase expression by higenamine, an active component of aconite root.

Effects of higenamine on nitric oxide (NO) production and inducible NO synthase (iNOS) mRNA expression (RAW 264.7 cells), on vascular reactivity in vitro and in vivo (rats), and on survival rates (mice) and serum nitrite/nitrate levels (rats) were investigated by using last lipopolysaccharide (LPS) plus interferon (IFN)-gamma. Higenamine concentration-dependently inhibited NO production and inducible NO synthase mRNA in RAW 264.7 cells, in which the IC(50) was 53 microM. Higenamine (10 mg/kg i.p.) administered 90 min before LPS (5 mg/kg i.v.) prevented not only LPS-induced hypotension but also pressor response to norepinephrine (1 microgram/kg) in rats. Incubation of thoracic aorta with LPS (300 ng/ml) for 8 h in vitro resulted in suppression of the vasoconstrictor effects to phenylephrine, which was prevented by coincubation with higenamine. The survival rate to endotoxin in mice was significantly (P <.01) increased by the presence of higenamine in the LPS-treated group up to 48 h. Serum nitrite/nitrate levels were significantly (P <.05) reduced by higenamine in LPS-treated rats. Finally, higenamine inhibited the activation of nuclear factor kappaB in RAW 264.7 cells due to LPS + IFN-gamma by mobility shift assays. Taken together, these data strongly suggest that higenamine inhibits iNOS expression by inhibiting nuclear factor kappaB activation by LPS + IFN-gamma, which may be beneficial in inflammatory diseases in which enhanced formation of NO is the main causative factor. Furthermore, due to positive inotropic action, higenamine may be more effective in a condition where myocardial contractility is likely to depress, such as in septic shock and/or endotoxin-induced inflammatory disorders.

Aconitum↗