Ginsenoside potentiates NO-mediated neurogenic vasodilatation of monkey cerebral arteries.
The aqueous extract of the Panax ginseng (GE) potentiated the relaxation induced by transmural electrical stimulation or nicotine in monkey cerebral arterial strips denuded of the endothelium and partially contracted with prostaglandin F(2 alpha). The response to electrical stimulation was abolished by tetrodotoxin, whereas that to nicotine was suppressed by hexamethonium. N(G)-nitro-L-arginine abolished both of the neurogenic relaxation. Atropine did not alter the potentiating effect of GE. Relaxations induced by exogenous NO were unaffected by GE. The enhancement by GE, of the neurogenic response, appears to be associated with increment in the synthesis or release of NO from the perivascular nerve. Blockade of muscarinic prejunctional inhibition, superoxide scavenging action and phosphodiesterase inhibition are not involved.
Toda
N
N
Department of Pharmacology, Shiga University of Medical Science, Seta, 520-2192, Ohtsu, Japan.
Ayajiki
K
K
Fujioka
H
H
Okamura
T
T
D000818:Animals; D002491:Central Nervous System Agents / Q000494:pharmacology*; D002536:Cerebral Arteries / Q000187:drug effects; D002851:Chromatography, High Pressure Liquid; D004357:Drug Synergism; D004558:Electric Stimulation; D005260:Female; D036145:Ginsenosides; D008251:Macaca; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology*; D010936:Plant Extracts / Q000494:pharmacology*; D012503:Saponins / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects*
D002491:Central Nervous System Agents; D036145:Ginsenosides; D010936:Plant Extracts; D012503:Saponins; D009569:Nitric Oxide