Drug-Induced ED

Erectile dysfunction is a common adverse effect of a number of drugs, and it often has a great effect on patient compliance. This subject as a risk factor is lightly discussed here and further discussed in more detail later in the textbook. It is important to recognize that many of the drugs associated with ED are used to treat conditions that are themselves risk factors for ED, thus the interpretation of ED in the setting of pharmacological therapy is often difficult in the clinical setting.

Selective Serotonin Reuptake Inhibitors

Selective serotonin reuptake inhibitors (SSRIs) have gained notoriety as a common cause of several manifestations of sexual dysfunction. SSRI-induced ED rather than sexual dysfunction, though, is rarely reported in the literature and is limited mostly to case reports.

Antihypertensive Agents

Several antihypertensive agents have been implicated in ED, yet the evidence is limited. Older thiazide diuretic treatments have been associated with mild effects on erectile function.

Many of these studies have limited clinical implications as they were conducted with chlorthalidone, a thiazide-like diuretic. A recent study suggested that beta-blocker-induced ED is likely psychogenic rather than organic. Clonidine is reported to cause ED in both human and animal studies through agonism of central alpha-2 adrenoreceptors.

Statins and Viagra online Canadian pharmacy

Statins are HMG-CoA reductase inhibitors that are a commonly used medication for the treatment of hyperlipidemia. Do et al. conducted a study to investigate the association between exposure to statins and the occurrence of ED. The study was limited to males age 18–30. They found a statistically significant association for statins with induction and worsening of ED. Further studies are needed to distinguish the severity of the effect on ED between the many different statin drugs that are currently in use.

Antipsychotics

Antipsychotic medications are also implicated in ED. These drugs exert their effects primarily by antagonism of dopamine receptors but have effects on several other receptors. In addition, dopamine antagonism causes hyperprolactinemia which contributes to the sexual dysfunction associated with these drugs.

Antiandrogens

Antiandrogens are a well-known cause of sexual dysfunction and ED. In recent studies, finasteride has been shown to cause minimal ED at higher doses (5 mg) for prostate cancer prevention, and almost no effect on erectile function at low doses (1 mg) for the treatment of alopecia.

Illicit Substances and Nicotine

Several illicit substances cause ED. In addition, men on methadone maintenance therapy for heroin dependence have been reported to have significant impairment of erectile function. The use of tobacco products, and specifically nicotine, is associated with ED in both chronic and acute exposure. Nicotine produces vasoconstriction through its actions on endothelial cells through a likely underproduction and degradation of nitric oxide. A recent study of healthy men between the ages of 18 and 27 reported that the use of nicotine gum immediately decreased erectile response to visual stimuli despite unchanged subjective measurements of sexual arousal. This study may imply an immediate neurogenic and hemodynamic response of the penile tissue to nicotine. Furthermore, chronic cigarette smoking is also associated with an independently increased risk of ED and clinically significant damage to penile vasculature.

Ethanol

The role of ethanol, while classically thought to impede erectile function, has been less clear in the literature. Sublingual viagra pharmacy Despite the association of alcohol consumption and sexual activity, very little objective evidence exists on the effect of acute ethanol intoxication on erectile function. The data on chronic ethanol exposure is also mixed. Ethanol exposure in an animal model showed histologic evidence of both endothelial damage and metabolic dysfunction. Impairment of smooth muscle relaxation due to endothelial dysfunction was pronounced while neurogenic smooth muscle relaxation remained intact.