On the horizon is gene therapy that would deliver genes that produce products or proteins that may not be functioning properly in the penile tissue of men with ED. Replacement of these proteins may result in improvement in erectile function. Experimental animal models have demonstrated improvement in erectile function with gene therapy. Human studies may also demonstrate success with this therapy. Gene therapy may take a long time for regulatory approval and public acceptance.


Multiple combinations of intracavernosal therapy exist and the effectiveness of them varies based on patient characteristics and varying dosing strength (Table 1). Combination therapy have been extremely effective in the SCI population, and have several advantages including a reduction in cost per dose and side effects base on the lowered dose of each component (101,102). Effectiveness of combination therapy in the spinal cord population is well established, but no specific dose recommendations can be made based on the data (103-106). The use of combination therapy on other forms of neurogenic ED have not been well studied, but there use can be trialed as second-line therapy, or for populations were the side effects of PDE5i may preclude use such as in MSA due to hypotension.
Factors that mediate contraction in the penis include noradrenaline, endothelin-1, neuropeptide Y, prostanoids, angiotensin II, and others not yet identified. Factors that mediate relaxation include acetylcholine, nitric oxide (NO), vasoactive intestinal polypeptide, pituitary adenylyl cyclase–activating peptide, calcitonin gene–related peptide, adrenomedullin, adenosine triphosphate, and adenosine prostanoids.
Erections are initiated and maintained via integration of afferent inputs in the supra sacral regions of the central nervous system. Regions of the brain cited to have key roles in the integration of signals include the medial amygdala, MPOA, periaqueductal gray matter, paraventricular nucleus (PVN), and ventral tegmentum among others (16). Studies in animal models, particularly in rats, have been paramount in identifying these key areas of signal integration and control. Electrostimulation of the MPOA, PVN and hippocampus lead to erection and lesions in these areas may prevent erection (17). Marson et al. injected labeled pseudorabies virus into rat corpora cavernosa and traced them to neurons in the spinal cord, brain stem and hypothalamus (18). Stimulation of the rat dorsal nerve led to increased firing in the MPOA not found elsewhere (19). Axonal tracing in animals have shows direct projections from the hypothalamus to the lumbosacral autonomic erection centers. Oxytocin and vasopressin have been identified as central neurotransmitters within the hypothalamic nuclei and may have a role in penile erection (17). These signaling studies identifying key areas of erectile response integration may explain how ED is associated with cerebrovascular accident (CVA), Parkinson’s, epilepsy and MS.
Caution is recommended regarding the use of PDE-5 inhibitors and alpha-blockers (for example, Hytrin, Cardura, Uroxatral, Flomax, Rapaflo), medications commonly used to treat benign prostate enlargement (BPH). The combination of these medications can cause lowering of the blood pressure. Stable use of one therapy should occur prior to the addition of the other therapy, which should start at a low dose.
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Society of Clinical Oncology, American Urological Association, Association of Women Surgeons, New York Academy of Sciences, Society of Government Service Urologists, Society of University Urologists, Society of Urology Chairpersons and Program Directors, and Society of Women in Urology
In some cases, however, these drugs may be unsuitable for patients with heart disease. If you are considering one of these drugs and you have heart disease, as many diabetics do, be sure to tell your doctor. In rare cases, the pills may create “priapism,” a prolonged and painful erection lasting six hours or more (although reversible with prompt medical attention).
Erectile dysfunction or ED (It used to be called impotence) is the inability to achieve or sustain an erection suitable for sexual intercourse. Problems with erections may stem from medications, chronic illnesses, poor blood flow to the penis, drinking too much alcohol, or being too tired. Erectile dysfunction can occur at any age, but it is more common in men older than 75.
Can erectile dysfunction be reversed? Erectile dysfunction (ED) is a very common issue, and it can usually be reversed with lifestyle changes, counseling, medications, or surgery. While short-term treatments are available, addressing the underlying cause will usually resolve the condition. Learn about causes and effective methods of reversing ED here. Read now
The inability to achieve or sustain a sufficiently firm penile erection (tumescence) to allow normal vaginal sexual intercourse. The great majority of cases are not caused by organic disease and most men experience occasional periods of impotence. It is often related to anxiety about performance and is usually readily corrected by simple counselling methods which prescribe sensual massage but forbid coitus. Organic impotence may be caused by DIABETES, MULTIPLE SCLEROSIS, spinal cord disorders and heart disease. Many cases can be helped by the drug SILDENAFIL (Viagra).

Viagra is available in three strengths: 25 mg, 50 mg, and 100 mg. Viagra works best if taken on an empty stomach about 30-45 minutes before sexual activity. Optimal results may not be realized until the medication has been tried six to eight times. Viagra may be used cautiously with alpha-blocker medications as long as sufficient time has passed between their dosing.
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Six herbs for treating erectile dysfunction Erectile dysfunction can be an embarrassing condition that can leave men unable to achieve an erection or a full orgasm. This MNT Knowledge Center article talks about six different herbal supplements that could help people with erectile dysfunction, including ginkgo biloba, horny goat weed, and red ginseng. Read now
If you bike a lot and have a very narrow saddle on your bicycle, consider switching to a "no-nose seat" which is wider at the back than a conventional saddle, allowing more of your weight to be distributed to the sitting bones. Make sure the seat is level or angled slightly downward and at a height that allows your knee to be just slightly bent at the bottom of the pedal cycle. Raising the handlebars on your bike so that you're sitting upright may also help.
When sexually stimulated there is a release of a chemical, nitric oxide (NO) in the blood vessels of the corpus cavernosum. The NO stimulates the production of a compound called cGMP, which causes relaxation of the smooth muscle in the blood vessels supplying the corpus cavernosum. PDE 5 is an enzyme that breaks down cGMP. By inhibiting the breakdown of cGMP by PDE5, these medications allow cGMP to build up in the penis. cGMP causes muscles in the corpora cavernosa of the penis to relax. When the muscle is relaxed, more blood can flow into the penis and fill the spaces in the penis. As the penis fills with blood, the veins in the penis are compressed, and this results a hard erection. When the effect on PDE5 decreases, the cGMP levels go down and the muscle in the penis contracts, causing less blood to flow into the penis and allowing the veins to open up and drain blood out of the penis.
3. Are there physical causes of erectile dysfunction? Erectile dysfunction may be a symptom of underlying medical conditions, which if not detected may cause further medical problems. A prior history of cigarette smoking, heart attacks, strokes, and poor circulation in the extremities (for example, intermittent claudication or cramping in your leg[s] when you walk) suggest atherosclerosis as the cause of the erectile dysfunction. Loss of sexual desire and drive, lack of sexual fantasies, gynecomastia (enlargement of breasts), and diminished facial hair suggest low testosterone levels. A prior history of pelvic surgery or radiation and trauma to the penis/pelvis/perineum can cause problems with the nerves and blood vessels. Symptoms of intermittent claudication of the lower extremities with exercise may suggest a vascular problem as a cause of the erectile dysfunction.

medicines called alpha-blockers such as Hytrin (terazosin
HCl), Flomax (tamsulosin HCl), Cardura (doxazosin
mesylate), Minipress (prazosin HCl), Uroxatral (alfuzosin HCl),
 Jalyn (dutasteride and tamsulosin HCl), or Rapaflo (silodosin).
Alpha-blockers are sometimes prescribed for prostate
problems or high blood pressure. In some patients, the use
of Sildenafil with alpha-blockers can lead to a drop in blood pressure or to fainting
Currently, placement of a penile prosthesis is the most common surgical procedure performed for erectile dysfunction. Penile prosthesis placement is typically reserved for men who have tried and failed (either from efficacy or tolerability) or have contraindications to other forms of therapy including PDE5 inhibitors, intraurethral alprostadil, and injection therapy.
The role of the endothelium in erectile function became clearer with the observation that the phosphodiesterase type 5 (PDE5) inhibitor, sildenafil, enhanced erectile function. Erection occurs with the release of nitric oxide (NO) from the vascular endothelial cells.17 The reduction in endothelial cell production of NO results in the negative impact on the smooth muscles in the corporal bodies and results in less relaxation of the smooth muscle cells with decrease in blood supply and resulting ED. A similar phenomenon is well known to impact the coronary arterial system resulting in CVD.
NO is produced by the enzyme NO synthase (NOS). [13] NOS plays many roles, ranging from homeostasis to immune system regulation. To date, 3 subtypes have been identified: nNOS, iNOS, and eNOS, which are produced by the genes NOS1, NOS2, and NOS3, respectively. This nomenclature is derived from the sources of the original isolates: neuronal tissue (nNOS), immunoactivated macrophage cell lines (iNOS), and vascular endothelium (eNOS). The subtypes are not, however, limited to the tissues from which they were first isolated.

Nearly every primary care physician, internist and geriatrician now understand that many older men retain an interest in sexual activity as they age. Some primary care physicians think that sexual potency in older men is the norm, and that if it is lacking, it is ‘all in the head.’ This viewpoint has not been supported by current literature. The Massachusetts Male Aging Study (MMAS) found that 52% of men between 40 and 70 years old reported having some form of erectile dysfunction (ED).1 The reality is that ED is a natural part of ageing and that the prevalence increases with age. In the MMAS, they found that roughly 50% of men at 50 years old, 60% of men at 60 years old and 70% of men at 70 years old had ED. Thus, nearly all men who live long enough should develop ED. The myths that surround the problems of impotence or ED confound the attempts of patients to receive treatment and the attempts of physicians to help them.1

ED usually has something physical behind it, particularly in older men. But psychological factors can be a factor in many cases of ED. Experts say stress, depression, poor self-esteem, and performance anxiety can short-circuit the process that leads to an erection. These factors can also make the problem worse in men whose ED stems from something physical.
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