Impotence, or erectile dysfunction, can be defined as the persistent inability to develop and/or maintain an erection adequate for sexual intercourse. Vascular diseases, including atherosclerosis, hypertension, diabetes, and high cholesterol, can cause restricted blood flow to the penis and may account for approximately 70% of physically related causes of erectile dysfunction . The arterial blood supply to the penis is mainly provided by the internal pudendal artery, which branches into several smaller arteries that contribute to vascularization of the erectile tissues. The erectile tissue of the human penis consists of two dorsal corpora cavernosa and a ventral corpus spongiosum. Reduced sympathetic input combined with stimulation
of parasympathetic pathways induces vascular smooth muscle relaxation and vessel dilation, causing increased arterial blood flow to the penis, engorgement of the erectile tissues, reduced venous outflow, and erection.
The physiological regulation of erectile function has been well reviewed [12-15]. To understand how ginseng may affect the erection process, a brief overview of ginseng-relevant processes will be described. The dilation of penile vascular smooth muscle is dependent on several neuronal pathways and vasoactive substances. The flaccid state of the penis is maintained by sympathetic nerve stimulation and the release of the adrenergic neurotransmitter norepinephrine, as well as by production of the vasoconstrictor endothelin-1 by vascular endothelial cells. Attenuated sympathetic input to the penis will decrease vasoconstrictive tone and allow vessel dilation. With increased parasympathetic nerve stimulation and the release of the cholinergic neurotransmitter acetylcholine and the peptide vasoactive intestinal peptide or VIP, there is a further increase in vasodilation. Another vasoactive substance, nitric oxide, is produced by nonadrenergic-noncholingeric (NANC) neurons that innervate penile vasculature. Acetylcholine-induced vasodilation is also mediated by nitric oxide. Nitric oxide (NO) is produced from L-arginine and oxygen by the enzyme nitric oxide synthase (NOS). Three isoforms of NOS have been elucidated: neuronal NOS (nNOS or NOS-1), inducible NOS (iNOS or NOS-2), and endothelial NOS (eNOS or NOS-3). Neurons that innervate the corpus cavernosa contain nNOS, while eNOS is localized in the endothelium and smooth muscle of the cavernosa. Inducible NOS does not appear to be involved in the physiology of erections, but may be a factor in the deleterious effects of aging on the delicate erectile tissues of the corpora cavernosa [16, 17]. Nitric oxide directly increases the enzyme guanylate cyclase, which catalyzes the conversion of guanosine triphosphate (GTP) to cyclic guanosine-3',5'-monophosphate (cGMP). The cyclic nucleotide cGMP is a second messenger that activates cGMP-dependent protein ki-nase, leading to decreased intracellular calcium, smooth muscle relaxation of the penile arterioles, and consequent increased blood flow into the erectile tissues. The shear forces induced by this increased blood flow against the endothelial cell surface and the increased pressure within the erectile tissues trigger eNOS and the production of more nitric oxide, thus reinforcing the turgidity of the penis. The cyclic nucleotide phosphodiesterases (PDE) located within the penile vasculature degrade cGMP by hydrolyzing cGMP into the inactive 5'-GMP. Oral phophodiesterase inhibitors can be prescribed to treat erectile dysfunction. These drugs include silde-nafil, vardenafil, and tadalafil, and when taken orally they selectively inhibit cGMP-specific phosphodiesterase type 5, the predominant phosphodiesterase isoform in the penis. By preventing cGMP breakdown and, consequently, increasing cGMP levels, these drugs help to promote penile vasodilation and can prolong and maintain erection.
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