title: Effects of ginsenosides on vasodilator nerve actions in the rat perfused mesentery are mediated by nitric oxide.
abstract: This study was designed to explore the effect of ginsenosides, saponins from Panax ginseng, on the vasodilator nerve actions in the rat perfused mesentery and the mechanism of this effect. In the rat perfusion mesentery, when adrenergic nerves were blocked by guanethidine (5 x 10(-6) M) and vascular muscle tone was increased with methoxamine (5 x 10(-6)-10(-5) M), transmural field stimulation produced a frequency-dependent vasodilator response, which is due to the release of calcitonin gene-related peptide; ginsenosides significantly suppressed this vasodilator response in a concentration-dependent manner (3-30 micrograms mL-1). After pretreatment with saponin (50 micrograms mL-1, 3 min) to damage endothelial cells, this suppressing effect of ginsenosides was unaltered. However, the effect was abolished by N omega-nitro-L-arginine methyl ester (L-NAME) (10(-4) M), an inhibitor of nitric oxide synthesis and addition of L-arginine (3 x 10(-4) M) restored this suppressing effect. Methylene blue (10(-5) M), an inhibitor of guanylate cyclase, also abolished the suppressing effect of ginsenosides. However, ginsenosides did not alter the relaxation responses caused by exogenous calcitonin gene-related peptide administration. We conclude that ginsenosides can produce an inhibitory effect on the vasodilator response prejunctionally in the rat perfused mesentery and that this effect of ginsenosides may be mediated by nitric oxide released from non-adrenergic, non-cholinergic nerves.
authors.affiliation: Department of Pharmacology, Hunan Medical University, P.R. China.
authors.forename: C F
authors.initials: CF
authors.lastname: Peng
authors.forename: Y J
authors.initials: YJ
authors.lastname: Li
authors.forename: Y J
authors.initials: YJ
authors.lastname: Li
authors.forename: H W
authors.initials: HW
authors.lastname: Deng
mesh_terms: D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D004730:Endothelium, Vascular / Q000187:drug effects; D036145:Ginsenosides; D006145:Guanethidine / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects* / Q000294:innervation; D008729:Methoxamine / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D005894:Panax / Q000378:metabolism*; D010477:Perfusion; D010946:Plants, Medicinal; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000494:pharmacology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D018663:Adrenergic Agents; D036145:Ginsenosides; D012503:Saponins; D014662:Vasoconstrictor Agents; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D008729:Methoxamine; D015740:Calcitonin Gene-Related Peptide; D019331:NG-Nitroarginine Methyl Ester; D006145:Guanethidine