Of particularly concern are antihypertensive medications for CVD (eg, digoxin, disopyramide [Norpace], gemfibrozil [Lopid]), anxiety, depression (eg, lithium, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants), or psychosis (eg, chlorpromazine, haloperidol, pimozide [Orap], thioridazine, thiothixene). Antihypertensive drugs, such as diuretics (eg, spironolactone, thiazides) and beta blockers, may be associated with ED. Discontinuation or switching to alternative drugs, such as angiotensin-converting enzyme inhibitors or calcium channel blockers (eg, diltiazem, nifedipine, amlodipine), may reduce ED. The newer angiotensin II receptor antagonists may be less problematic with respect to ED, but long-term data is needed to evaluate this.
Sexual stimulation causes the release of neurotransmitters from cavernosal nerve endings and relaxation factors from endothelial cells lining the sinusoids. NOS produces NO from L-arginine, and this, in turn, produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP), which work via calcium channel and protein kinase mechanisms (see the image below). This results in the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a dramatic increase in penile blood flow.
A study published in May 2014 in The Journal of Sexual Medicine found that some men can reverse erectile dysfunction with healthy lifestyle changes, such as exercise, weight loss, a varied diet, and good sleep. The Australian researchers also showed that even if erectile dysfunction medication is required, it's likely to be more effective if you implement these healthy lifestyle changes.
Erectile dysfunction (ED) is one of the most common conditions affecting middle-aged and older men. Nearly every primary care physician, internist and geriatrician will be called upon to manage this condition or to make referrals to urologists, endocrinologists and cardiologists who will assist in the treatment of ED. This article will briefly discuss the diagnosis and management of ED. In addition, emerging concepts in ED management will be discussed, such as the use of testosterone to treat ED, the role of the endothelium in men with ED and treating the partner of the man with ED. Finally, future potential therapies for ED will be discussed.
In fact, one study showed that men who use these medications recreationally, when they’re not really needed, were more likely to develop psychological impotence! Therefore, instead of wasting money, risking one’s physical health and worsening one’s erectile function, men with psychological impotence should opt for treatment strategies that truly address the root of the trouble.
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.
Induction of erection occurs after stimulation of the cavernous and pelvic nerve plexus. Conversely, stimulation of the sympathetic trunk leads to detumescence. The reflex erectile response requires that the sacral reflex arc remain intact. Tactile and sensory signals are received by the somatic sensory pathways and integrate with parasympathetic nuclei within the sacral spinal cord (S2-4) leading to induction of erection via cholinergic signaling. These reflexogenic erections remain intact with upper motor neuron injuries. Psychogenic erections do not require that the sacral reflex arc remain intact. In a cat models, spinal cord removal below L4/L5 led to absence of a reflexogenic erection but stimulation of the medial preoptic area (MPOA) or placement near a female cat in heat led to erection (5,6). Psychogenic erections occur via induction of central pathways traveling from the brain through the sympathetic chain. Non-penile sensory pathways induced by sight, sound, touch and smell travel through the MPOA to the erection centers within the cord T11-L2, and S2-S4 to induce erections (7). When a sacral lower motor neuron injury is present in men, below T12 these types of erections are more likely to occur (8). Spinal cord lesions above T9 are not associated with psychogenic erections (9). Rigidity of erections is less with psychogenic erections because the thoracolumbar sympathetic outflow may contain a decreased concentration of neurons compared to the parasympathetic outflow from the sacral spinal cord.
Can’t or don’t want to take ED drugs? The vacuum pump method is the next most common choice among men with erectile dysfunction who pass on pills, says Dr. Bennett. To create an erection, you place a plastic cylinder over the penis and pump the air out of the cylinder to force blood to flow into the penis. An elastic ring that you slide onto the base of your penis holds the erection. This ED treatment device is effective for about 75 percent of men. Side effects include numbness, bruising, and weak ejaculation — and the ring must be removed after 30 minutes.
Trauma to the pelvic blood vessels or nerves can also lead result in ED. Bicycle riding for long periods has been implicated as an etiologic factor; direct compression of the perineum by the bicycle seat may cause vascular and nerve injury.  On the other hand, bicycling for less than 3 hours per week may be somewhat protective against ED.  Some of the newer bicycle seats have been designed to diminish pressure on the perineum. [37, 38]
Do erectile dysfunction exercises help? Many people have erectile dysfunction (ED), but it is often possible to reverse this with exercises to strengthen muscles in the area. These include pelvic floor exercises. ED can often be due to lifestyle factors including obesity and low physical activity levels. Learn more about exercises for ED here. Read now
In one study, 9.6% reported ‘occasional’ erectile dysfunction, 8.9% reported erectile dysfunction occurring ‘often’, and 18.6% reported erectile dysfunction occurring ‘all the time’. Of these, only 11.6% had received treatment.In another study, only 14.1% of men reported that they had received treatment, despite experiencing erectile dysfunction for longer than 12 months.
The sympathetic pathway originates from the 11th thoracic to the 2nd lumbar spinal segments and goes via the white rami to enter the sympathetic chain ganglia. Subsequently nerves travel through the lumbar splanchnic to inferior mesenteric and superior hypogastric nerves to the pelvic plexus. The T10 through T12 segments are most often the origin of sympathetic fibers, and the sympathetic chain ganglia that innervate the penis are located in the sacral and caudal ganglia (3).
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).
There are risks to prosthetic surgery and patients are counselled before the procedure. If there is a post-operative infection, the implant will likely be removed. The devices are reliable, but in the case of mechanical malfunction, the device or a part of the device will need to be replaced surgically. If a penile prosthesis is removed, other non-surgical treatments may no longer work.