**1. Introduction**

Erectile dysfunction (ED) or (male) impotence is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis [1]. There are various underlying causes, such as a compromised cardiovascular system and diseases such as diabetes and chronic kidney disease (CKD), many of which are medically treatable. The causes of erectile dysfunction may be physiological or psychological [2]. Sexual function includes libido, penile erection, ejaculation, and orgasm. While each of these parameters may be of concern to an individual patient, the vast majority of men complain of ED. Testosterone deficiency frequently is associated with decreased libido and ED. ED is a clinical problem that is underdiagnosed, under-evaluated, and under-treated. The prevalence of ED increases with age, and it is associated with multiple medical conditions including diabetes, hypertension, and heart disease that also increase with age. ED is a highly prevalent and often underreported condition. The prevalence of ED varies in different countries and approximately 100 million men worldwide are estimated to be affected with ED. More than half of US men between the ages of 40 and 70 years are estimated to have ED. The worldwide ED prevalence in men with diabetes ranges from 27% to 75% and it is estimated that the prevalence of ED will double in the next 25 years [3]. There is a strong link between ED and atherosclerotic disease due to the fact that they share similar risk factors. In a study where patients referred for myocardial perfusion single-photon emission computed tomography were screened for ED with a questionnaire, it was found out that 54.8% of the patients had ED. Patients with ED showed more severe coronary heart disease. In diabetic patients, ED has been shown to predict silent coronary artery disease, and in asymptomatic men without cardiovascular risk factors or

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known vascular disease [4]. Nevertheless, the hypothesis that ED, as a manifestation of autonomic neuropathy, may be linked with the lack of symptoms in a proportion of diabetic patients with silent CAD cannot be excluded [4].

**2.1. Aging**

decrease of blood flow contributes to ED.

cells, and synthesis or activity of NO [12].

**2.2. Oxidative stress**

Aging has been considered to be one of the major reasons for decreased sexual functions, which are also affected by a change in lifestyle, increased day-to-day stress, depression, diabetes and/ or other metabolic and endocrine disorders. Various medications such as antidepressants, tranquilizers, hypnotics, antiandrogens and antihypertensive agents can also lead to the downfall of the sexual functions [6, 7]. There is a close relationship between aging and ED [8]. Research shows that chances of developing ED increase with age and are due to several agerelated factors such as a reduction in nonadrenergic noncholinergic nerve endings in the penis and decreased endothelial nitric oxide (eNOS) activity. The decreased activity of eNOS and bioavailability of NO impairs corpus cavernosum relaxation which can be exacerbated by an increased release of vasoconstrictors. These confounding events are responsible for the increase in the contractile tone in the penile vasculature [9]. Testosterone is secreted in a circadian manner in younger men, but diurnal fluctuation is reduced and may disappear in aging men [10]. Whatever the initiating factor of ED, the ultimate common pathological process is damage to smooth-muscle cells and an increase in the accumulation of fibrosis, which decrease the vasodilator response. This increased accumulation of collagen with aging has been observed in both human and rat corporal smooth muscle [11]. The increase in collagen accumulation leads to a decrease in blood flow as measured by peak systolic velocity, and this

Potentials of Phytotherapeutic Treatment of Erectile Dysfunction

http://dx.doi.org/10.5772/57174

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As men age, dysfunction of this complex process occurs with an increased incidence and prevalence. The cause of this age-related erectile dysfunction is not well understood and likely involves multifactorial alterations in the cavernosal endothelial cell lining, smooth muscle

Oxidative stress (OS) is one of the major contributory factors towards ED. There is a growing interest among researchers regarding the role of oxidative stress in the pathophysiological mechanism of ED. Oxidative stress occurs when there is an imbalance between pro-oxidants and the ability of the antioxidants to scavenge excess reactive oxygen species (ROS) [3]. Penile erectile tissue is formed by 2 dorsal corporal bodies known as the corpora cavernosa. The cavernosal bodies are composed of sinusoidal spaces with a trabecular meshwork. These spaces are lined by endothelium. Neural transmitters, such as acetylcholine, are released from cavernosal nerve endings and stimulate the neuronal NOS (nNOS) enzyme, which leads to the release of NO from the endothelium. Erectile function is mediated by both nNOS and endo‐ thelial NOS (eNOS) [13]. NO is the principal mediator of penile erection [13]. Erectile function is dependent on relaxation of the cavernous smooth muscle, and its mechanism of action is dependent on penile smooth muscle relaxation, mediated by NO. Decreased production or absence of NO may play a major role in ED. Production decreases when the availability of substrate for NOS is reduced. NO is a highly reactive free radical that undergoes nonenzymatic reaction with the heme moiety of oxyhemoglobin or that reacts with free radicals, such as superoxide anion, to form peroxynitrite [14]. The relationship between OS in the penis and age related ED has only been recently investigated and it was shown that as one ages, free radicals
