Laboratory studies indicate a role for NO in mediating many of the actions of ginseng and ginsenosides on copulatory performance. In rats treated for 3 months with oral ginseng extract versus no treatment, there was significantly increased intra-cavernosal pressure following stimulation of pelvic nerves innervating the corpus cavernosum . Ginsenoside-containing extracts of P. ginseng produced a dose-related increase in cGMP and endothelium-dependent dilation and relaxation of penile corpus cavernosum in rabbit [28,29]; treatment with the NOS inhibitor N-nitro-L-arginine blocked the ability of ginseng to induce this relaxation. Ginseng extract also enhanced acetylcholine-induced and transmural nerve-stimulation-elicited relaxations in rabbit corpus cavernosum tissue and reversed phenylephrine-induced corpus cavernosum smooth muscle vasoconstriction . Both the neurogenic and endothelium-mediated relaxations were enhanced by superoxide dismutase (SOD), a scavenger of the superoxide anion that inactivates NO, and were blocked by N-nitro-L-arginine and oxyHb, compounds that inhibit NOS and trap NO, respectively . Ginseng/ginsenosides modulate vasoactivity in a number of other systems as well . Ginseng extract and ginsenosides Rg3, Rg1, Re, and Rb1 have been shown to increase NOS activity and NO production and increase cGMP levels in cardiomyocytes  and in aortic, pulmonary, cerebral and umbilical endothelial cell cultures  and have been postulated to offer both neuro- and cardiovascular protection [33, 34].
The exact mechanisms by which ginseng/ginsenosides stimulate NOS and NO release remain unclear. As shown in Fig. 4.1, the ginsenoside structure contains polar and nonpolar regions that may allow ginsenosides to intercalate into cell plasma membranes and alter membrane fluidity and cell signaling [1, 35]. There is also evidence that ginsenosides may interact with steroid hormone receptors and stimulate NO production through nongenomic, transcription-independent mechanisms of action . Steroidal estrogens, androgens, and corticosteroids are potent vasoactive modulators that can influence NO production through binding to their respective receptors [36-38]. Several ginsenosides have been reported to exert steroidlike activity, notably Rb1, Re, and Rg1 . Through binding to estrogen receptors, ginsenoside Re increased PI3-kinase/Akt and eNOS activity in arterial smooth muscle A10 cells, and the estrogen receptor antagonist ICI 182,780 blocked this ginsenoside Re action . While ginsenoside Re induced eNOS activity and NO production in cardiac myocytes, Re did not activate gene transcription and its effects on NO were blocked by concomitant treatment with estrogen, progesterone, and androgen receptor antagonists indicating a nongenomic action of Re on sex-steroid receptors . Similarly, ginsenosides Re and Rg1 have been shown to be functional ligands for the glucocorticoid receptor in human umbilical vein endothelial cells , producing a rapid Ca2+ influx, activation of the PI3-kinase/Akt pathways, and NO production that was abolished by treatment with a glucocorticoid receptor antagonist or siRNA targeting of the receptor . Through a nongenomic action on androgen receptors, ginsenoside Rb1 produce a rapid increase in eNOS expression and NO production in human aortic endothelial cells that was prevented by treatment with an androgen-receptor antagonist or inhibitors for the PI3-kinase/Akt and MEK/ERK pathways .
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