The neurovascular mechanism of erection is complex and involves multiple factors including hormones, neurotransmitters, elements of the autonomic nervous system (sympathetic and parasympathetic) and vasodilators such as NO. The common causes of ED include psychogenic disturbance with failure to relax cavernous smooth muscle, arterial insufficiency as a result of atheromatous disease, damage to the parasympathetic nervous system, spinal cord injury, diabetes or following pelvic surgery such as radical prostatectomy, radical cystectomy or bowel resection . It is important to note that cavernous nerves are unique in that although they belong to the autonomic nerves system they do not release either acetylcholine (Ach) or norepinephrine; however, they release NO in the penis. NO relaxes the smooth muscle of the corpora cavernosa via cyclic GMP (cGMP), allowing expansion of the cavernosal lacunar spaces, blood flow and erection. Thus, NO is not a direct dilator of the smooth muscle of cavernosal bodies, but it is an important mediator in this process. Erectile function may also be adversely affected by cigarette smoking, excess alcohol consumption, obesity and systemic diseases such as mononucleosis, hepatitis, HIV and cancer. Some men are prone to develop an erection that fails to subside after ejaculation (ie, priapism). The condition is associated with sickle-cell disease and leukemia, or may be a result of intracavernosal injection of drugs such as prostaglandin E1 . Peyronie’s disease causes a physical bend in the erect penis and also contributes to ED.
A combination of yohimbine and L-arginine is shown to significantly improve erectile function in people with ED. L-arginine is an amino acid that helps expand blood vessels. It’s regarded as safe and effective for ED but can cause side effects like nausea, diarrhea, and stomach cramps. Avoid taking L-arginine with Viagra, nitrates, or any high blood pressure medications.
Currently, there are four orally active drugs are available to treat ED. These include: sildenafil citrate (Viagra [Pfizer, USA]), vardenafil hydrochloride (Levitra [Bayer, Germany]), tadalafil (Cialis [Eli Lilly, USA]) and avanafil (Stendra, Spedra [Vivus Inc, USA]). These drugs inhibit the enzyme phosphodiesterase type 5 (PDE-5), which is responsible for the hydrolysis of cGMP. PDE-5 inhibitors and cGMP act as effectors of dilation of smooth muscle of cavernosal bodies. PDE-5 inhibitors are contraindicated in patients taking any kind of nitrate therapy for angina, and may not be appropriate for men with certain health conditions, such as severe heart disease, heart failure, history of stroke or heart attack, uncontrolled high blood pressure or diabetes, and patients with pigmental retinopathy. PDE-5 inhibitors are less effective in men with diabetes and men who have been treated for prostate cancer. PDE-5 inhibitors are also not effective in men with retinitis pigmentosa, a genetic disease involving PDE-5 deficiency. The common side effects of PDE-5 inhibitors include gastrointestinal upset, headache, nasal congestion, back pain and dizziness. The PDE-5 inhibitors may interact with other medications including antihypertension drugs. Nonetheless, the PDE-5 inhibitors are generally safe and effective for most men. The primary mechanism of action of these drugs is through the mediation of NO. NO is one of the key molecules involved in ED. It is a short-lived, highly permeable, pleiotropic, gaseous molecule, secreted from the postganglionic cavernosal parasympathetic nerves, endothelium of the cavernosal blood vessels, platelets in the cavernosal sinuses and phagocytic cells (monocytes, macrophages and neutrophils). NO acts on platelets to inhibit platelets adhesion and aggregation. NO causes relaxation of the smooth muscle of the cavernosal blood vessels of the penis, leading to vasodilation, tumescence and stimulation. Release of NO in the corpus cavernosum of the penis during stimulation activates the enzyme guanylate cyclase, which results in increased levels of cGMP, producing smooth muscle relaxation in the corpus cavernosum and resulting in increased blood flow (5). NO is mainly produced from cavernosal nerves, which are nonadrenergic, noncholinergic nerves within the penis, and acting via its second messenger cGMP. It has been suggested that maintaining normal body weight and mild exercise, as well as dietary supplementation of folic acid, zinc, calcium, vitamin C, vitamin E and L-arginine, a precursor of NO, can support the biochemical pathway leading to NO release . NO is an effector molecule that is involved in a number of intracellular functions such as vasorelaxation, endothelial regeneration, inhibition of leukocyte chemotaxis and platelet adhesion . A small proportion of autonomic nerves do not release either Ach or norepinephrine . For example, the cavernous nerves predominantly release NO in the penis. The exact mechanism is not known, but it is believed to be through increased intracellular calcium. Another gaseous molecule produced in the corpora cavernosa is hydrogen sulphide (H2S), which is also known to be involved in erectile function . H2S activates ATP-sensitive potassium channels in smooth muscle cells. Some reports indicate that NO acts in large vessels and H2S in small vessels. A high level of tumour necrosis factor-alpha has been shown in ED patients . Although current ED therapies using PDE-5 inhibitors are safe and effective, approximately 40% of ED patients do not respond to currently available treatment [11,12]. For these patients, herbal therapy may be useful.
Just because a product claims to be natural doesn't mean it's safe. Many herbal remedies and dietary supplements can cause side effects and dangerous interactions when taken with certain medications. Talk to your doctor before you try an alternative treatment for erectile dysfunction — especially if you're taking medications or you have a chronic health problem such as heart disease or diabetes.