Oral ED medication is considered highly effective and studies show it works on the majority of men. But no medication works for everyone and ED medication is no exception. Everyone’s reaction to a medication is unique and anything potent enough to help is strong enough to have side effects. If the medication isn’t working, it is important to tell your doctor. Sometimes it is a matter of needing a higher dose. Also, it has been shown that it takes 6 to 8 tries using the medication to experience the best result.
PD is a chronic neurodegenerative disease characterized by “motor” and “non-motor” symptoms that lead to progressive disability. Erectile and SD are “non-motor” symptoms and can occur in 50–69% of males with PD (39-42). Ejaculatory and orgasmic function are also impaired. PD affects the dopaminergic pathways leading to erection and arousal. Dopaminergic therapy for PD can improve ED, and sometimes therapy may lead to hypersexuality (43,44). A comparison of married men with PD to age matched controls with non-neurologic chronic disease such as arthritis did not show any discrepancy in ED rates (45). This suggests that ED in certain groups with PD may occur from disease related factors common in chronic illness, in general.
The first step in treating the patient with ED is to take a thorough sexual, medical, and psychosocial history. Questionnaires are available to assist clinicians in obtaining important patient data. (See Presentation.) Successful treatment of sexual dysfunction has been demonstrated to improve sexual intimacy and satisfaction, improve sexual aspects of quality of life, improve overall quality of life, and relieve symptoms of depression. (See Treatment.)
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.
Clinical experience in switching medications to improve ED has been disappointing in that improvement does not often occur. Nonetheless, it is important to try to discontinue possible offending medications before proceeding to more invasive ED treatment options. Oral ED medications have changed the way clinicians discontinue medications in patients with ED and has improved the approach. For example, a patient may develop ED on a thiazide diuretic. The diuretic may be withdrawn, but a trial of oral ED therapy can be initiated during the observation period while the patient is waiting to see if any spontaneous improvement in ED occurs after drug withdrawal. Alternatively, if diuretic therapy is effective, well tolerated, and controlling blood pressure, oral ED therapy can be used on an ongoing basis to treat the side effect of ED.
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Finally, there are NO-releasing polymers that are capable of delivering NO in a pharmacologically useful way. Such compounds include compounds that release NO upon being metabolised and compounds that release NO spontaneously in aqueous solution. Initial animal studies suggest that cavernosal injections of NO polymers can significantly improve erectile function.48
Surgery: If neither drugs nor the vacuum pump works, your doctor may suggest surgery. With surgery, the doctor can place a device in your penis that will cause enough hardness for intercourse. In a few cases, infections may develop after the operation, and the doctor may have to remove the device. Another operation that may help you is rebuilding the blood vessels in the penis to increase blood flow into the penis or decrease blood flow out of the penis. These procedures can help you to get and maintain an erection.
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.
Communicate with your partner. Do you feel comfortable and accepted when it comes to your sexual performance? If you're worried about meeting your partner's too-high expectations or living up to some kind of standard, it will be harder to maintain an erection - it's called performance anxiety. If you think your partner's judgment might be hindering your ability to have satisfying sex, you need to communicate your needs and find ways to make your sexual environment more inviting.
According to whom? What's the source of your statistic? Because it sounds astonishingly high, for me to get erections and then lose them. If what you are talking about is men not being able to get erections, why don't you be honest and say that normally this is completely associated with age (say, over-60, and especially over 75), and that the Viagra-class of medications is the simplest and easiest response.
One study examined the role of testosterone supplementation in hypogonadal men with ED. These men were considered nonresponders to sildenafil, and their erections were monitored by assessing nocturnal penile tumescence (NPT). After these men were given testosterone transdermally for 6 months, the number of NPTs increased, as did the maximum rigidity with sildenafil.  This study suggests that a certain level of testosterone may be necessary for PDE5 inhibitors to function properly.
VIP is a neurotransmitter with regulatory actions on blood flow, secretion and muscle tone with intracorporal adenylate cyclase activation and smooth muscle relaxation. VIP has been shown to elevate cAMP intracellular concentrations without affecting cGMP levels. However, when VIP is given alone it may not induce erection and requires combination with phentolamine or papaverine for it to be effective (88). Common associated adverse effects were facial flushing and headache. VIP in combination with phentolamine is currently being used in the UK and Europe and is seeking regulatory approval for use in the United States.
Tests such as the bulbocavernosus reflex test are used to determine if there is sufficient nerve sensation in the penis. The physician squeezes the glans (head) of the penis, which immediately causes the anus to contract if nerve function is normal. A physician measures the latency between squeeze and contraction by observing the anal sphincter or by feeling it with a gloved finger inserted past the anus.
Another potential new treatment consists of penile low-intensity shock wave lithotripsy. This consists of 1500 shocks twice a week for 3–6 weeks. The purpose is to stimulate neovascularisation to the corporal bodies with improvement in penile blood flow and endothelial function. The use of low-intensity shock wave lithotripsy may convert PDE5 inhibitor non-responders to responders.47
The main surgical treatment of ED involves insertion of a penile implant (also called penile prostheses). Because penile vascular surgery is not recommended for aging males who have failed oral PDE5 inhibitors, ICI or IU therapies, implants are the next step for these patients. Although placement of a penile implant is a surgery which carries risks, they have the highest rates of success and satisfaction among ED treatment options.