Erectile dysfunction is often assumed to be a natural concomitant of the aging process, to be tolerated along with other conditions associated with aging. This assumption may not be entirely correct. For the elderly and for others, erectile dysfunction may occur as a consequence of specific illnesses or of medical treatment for certain illnesses, resulting in fear, loss of image and self-confidence, and depression.
*All medications have both common (generic) and brand names. The brand name is what a specific manufacturer calls the product (e.g., Tylenol®). The common name is the medical name for the medication (e.g., acetaminophen). A medication may have many brand names, but only one common name. This article lists medications by their common names. For information on a given medication, check our Drug Information database. For more information on brand names, speak with your doctor or pharmacist.
This consensus development conference on male erectile dysfunction has provided an overview of current knowledge on the prevalence, etiology, pathophysiology, diagnosis, and management of this condition. The growing individual and societal awareness and open acknowledgment of the problem have led to increased interest and resultant explosion of knowledge in each of these areas. Research on this condition has produced many controversies, which also were expressed at this conference. Numerous questions were identified that may serve as foci for future research directions. These will depend on the development of precise agreement among investigators and clinicians in this field on the definition of what constitutes erectile dysfunction, and what factors in its multifaceted nature contribute to its expression. In addition, further investigation of these issues will require collaborative efforts of basic science investigators and clinicians from the spectrum of relevant disciplines and the rigorous application of appropriate research principles in designing studies to obtain further knowledge and to promote understanding of the various aspects of this condition.
If you are taking medications (alpha-blockers) for problems with an enlarged prostate, you should discuss your prostate medications with your doctor. Alpha-blockers also can cause lowering of the blood pressure. Thus your doctor will need to carefully watch your blood pressure when you start the PDE5 inhibitor. Common alpha-blockers include doxazosin (Cardura), terazosin (Hytrin), and tamsulosin (Flomax).
Impotence, also called erectile dysfunction, in general, the inability of a man to achieve or maintain penile erection and hence the inability to participate fully in sexual intercourse. In its broadest sense the term impotence refers to the inability to become sexually aroused; in this sense it can apply to women as well as to men. In common practice, however, the term has traditionally been used to describe only male sexual dysfunctions. Professional sex therapists, while they identify two distinct dysfunctions as forms of impotence, prefer not to use the term impotence per se. Thus, because of its pejorative connotation in lay usage and because of confusion about its definition, the word impotence has been eliminated from the technical vocabulary in favour of the term “erectile dysfunction.”
Normal erectile function depends on the release of NO and endothelial-dependent vasodilation of the penile arteries. The ‘artery size’ hypothesis, first described by Dr Montorsi, offers an explanation why men are more likely to develop ED before a myocardial infacrtion. It is believed that atherosclerosis affects all vascular beds equally but smaller arteries are more likely to become occluded than larger arteries.31 32 The penile arteries are 1–2 mm while the coronary arteries are 3–4 mm. Thus, the same degree of endothelial dysfunction and atherosclerosis is more likely to occlude blood flow in the penile arteries compared with the coronary arteries. The penile arteries therefore serve as a sensitive indicator for subsequent CVD. This theory is supported by the fact that ED occurs approximately 3 years prior to cardiac symptoms in virtually all patients with chronic coronary syndrome whereas patients with acute coronary syndrome have a much lower prevalence of sexual dysfunction.32

Picture this: you have the girl of your dreams laid out before you. You’re kissing and things are getting hot and heavy. There’s just one problem: you can’t get hard. Your thoughts quickly turn from “this is amazing” to “this is a disaster,” and before you know it, the story of your floppy dick is making its way down your lover’s social circle. That is if she’s an insensitive gossip. Either way, not being able to get a boner when the time is right is beyond embarrassing.

Inside the cell, NOS catalyzes the oxidation of L-arginine to NO and L-citrulline. Endogenous blockers of this pathway have been identified. The gaseous NO that is produced acts as a neurotransmitter or paracrine messenger. Its biologic half-life is only 5 seconds. NO may act within the cell or diffuse and interact with nearby target cells. In the corpora cavernosa, NO activates guanylate cyclase, which in turn increases cyclic guanosine monophosphate (cGMP). Relaxation of vascular smooth muscles by cGMP leads to vasodilation and increased blood flow.

Conditions that may be associated with ED include diabetes, [25, 26, 27] hypertension, [28] , and CAD, as well as neurologic disorders, endocrinopathies, benign prostatic hyperplasia, [29] , sleep apnea [30] , COPD, [31] and depression (see Table 1 below). [32, 33, 34, 35] In fact, almost any disease may affect erectile function by altering the nervous, vascular, or hormonal systems. Various diseases may produce changes in the smooth muscle tissue of the corpora cavernosa or influence the patient’s psychological mood and behavior.
It is important that physicians and other health care providers treating patients for chronic conditions periodically inquire into the sexual functioning of their patients and be prepared to offer counsel for those who experience erectile difficulties. Lack of sexual knowledge and anxiety about sexual performance are common contributing factors to erectile dysfunction. Education and reassurance may be helpful in preventing the cascade into serious erectile failure in individuals who experience minor erectile difficulty due to medications or common changes in erectile functioning associated with chronic illnesses or with aging.
Endocrine evaluation consisting of a morning serum testosterone is generally indicated. Measurement of serum prolactin may be indicated. A low testosterone level merits repeat measurement together with assessment of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin levels. Other tests may be helpful in excluding unrecognized systemic disease and include a complete blood count, urinalysis, creatinine, lipid profile, fasting blood sugar, and thyroid function studies.

All NOS subtypes produce NO, but each may play a different biologic role in various tissues. nNOS and eNOS are considered constitutive forms because they share biochemical features: They are calcium-dependent, they require calmodulin and reduced nicotinamide adenine dinucleotide phosphate for catalytic activity, and they are competitively inhibited by arginine derivatives. nNOS is involved in the regulation of neurotransmission, and eNOS is involved in the regulation of blood flow.
Exercise and lifestyle modifications may improve erectile function. Weight loss may help by decreasing inflammation, increasing testosterone, and improving self-esteem. Patients should be educated to increase activity, reduce weight, and stop smoking, as these efforts can improve or restore erectile function in men without comorbidities. Precise glycemic control in diabetic patients and pharmacologic treatment of hypertension may be important in preventing or reducing sexual dysfunction. [49]
The mechanisms by which testosterone plays a role in erectile function are not completely understood. A study evaluating the effect of testosterone on erections in surgically castrated rabbits and control animals, in which the rabbits’ intracavernosal pressures were compared after cavernosal nerve stimulation, determined that castrated rabbits had much lower pressures after stimulation than control rabbits did. [21] Notably, the pressures increased when castrated rabbits received exogenous testosterone replacement.
You're not hard. You're about to have sex for the first time with your date, who's truly beautiful. All you want to do is present your glorious, super strong erection and let it do the talking. And yet when you look down, you're limp instead of hard. This doesn't make any sense! you think. Every element you could possibly need for an erection is here. Nudity, beauty, passion, the tantalizing thrill of boning someone for the first time, and a little bit of booze to take the edge off. What on earth is wrong and why are you so unlucky? You turn to your date. "I swear, this never happens..."

Sexual dysfunction and ED become more common as men age. The percentage of complete ED increases from 5% to 15% as age increases from 40 to 70 years. But this does not mean growing older is the end of your sex life. ED can be treated at any age. Also, ED may be more common in Hispanic men and in those with a history of diabetes, obesity, smoking, and hypertension. Research shows that African-American men sought medical care for ED twice the rate of other racial groups.