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Sildenafil was originally developed for heart disease, but was found to have a unique mechanism of action that targeted only factors in the penis, even though it is taken orally. The rationale for the use of sildenafil is based upon the role of nitric oxide-induced vasodilation (which is mediated by cyclic GMP) in initiating and maintaining an erection.
In order to understand the action of sildenafil as well as some of its side effects, it would be worthwhile to briefly recall the physiology of penile erection. With sexual arousal through imaginative, visual, auditory, tactile, olfactory, and other erotic stimuli, nitric oxide (NO) is released by nonadrenergic, noncholinergic (NANC) neurons.
Dilation of the helicine arterioles and relaxation of the sinusoids lead to engorgement of sinusoidal spaces with blood.
The intracellular decline in Ca++ ions suppresses the activity of myosin light chain (MLC) kinase and thus increases the intracellular content of dephosphorylated MLC, which enables the smooth muscle cell to relax.
The PDEs are responsible for enzymatic degradation of the biologically active cGMP and cAMP to the biological inactive molecules GMP and AMP. The prototype of this new class of selective PDE5 inhibitors for the treatment of ED was sildenafil. This is a  disorder of the persistent inability to attain or maintain penile erection sufficient for sexual intercourse,affects millions of men to various degrees. The penis consists of two parallel cylinders of erectile tissue, the corpora cavernosa (which has a mesh work of vascular endothelium), and a smaller,single ventrally placed cylinder,the corpus spongiosum, which surrounds the urethra and distally forms the glans penis.Venous drainage of the erectile bodies occurs via postcavernous venules draining into the deep dorsal vein.
In the flaccid penis, a balance exists between blood flow in and out of the erectile bodies. In addition to diabetes, kidney disease, chronic alcoholism, multiple sclerosis, atherosclerosis, and vascular disease account for about 70 percent of all cases of ED. As mental tension leads to adrenaline production, the tissues are getting constricted preventing the erection. Medication: ED is also a side effect of many common drugs, including prescription and over-the-counter medications and illegal drugs. But Alcohol is a depressant, and, when consumed in more than small amounts, it really reduces the ability to have an erection. Nicotine directly interferes with the nerve pathways that produce and maintain an erection, and tobacco smoke causes heart disease and circulatory problems that reduce the supply of blood to the penis and destroy the flexibility of tissues. Due to sedentary  life style and increased intake of fatty food leads to blocking of arteries with fat deposits.
The one of the common misconception is that ED is a part of aging and has to be accepted as such.
Tags: #1565 Buy Generic Levitra Sample, vardenafil 20mg tab - snyders drug store before Erectile Dysfunction Drugs Viagra, cvs caremark pharmacy - Erectile Dysfunction Medication Reviews in Newfoundland, tadalafil how to take, Independent Pharmacy For Sale on account of sildenafil price till buy plavix online. Sildenafil is the first orally administered treatment of proven efficacy for erectile dysfunction.
Detumescence is associated with catabolism of cyclic GMP by type 5 cyclic GMP phosphodiesterase. Originally termed endothelial-derived relaxing factor, NO is known to be the most important physiologically occurring vasoactive molecule in the entire cardiovascular system. Expansion against the tunica albuginea compresses blood-draining subtunical venules, resulting in blockade of cavernous venous outflow.

It is well established that NO and cGMP are the most important transmitters for onset and maintenance of erection. Although some events in the cascade resulting in penile erection await clarification, NO, a gas with intrinsic vasodilator properties, activates guanylate cyclase and in turn stimulates the formation of cGMP This substance then acts as a second messenger, playing a pivotal role in vasodilatation and relaxation of corporal smooth muscle, the structural changes responsible for penile erection. PDE5 and, to a much lesser extent, PDE2 and PDE3, are localized to the corpus cavernosum of the penis, where they catalyze the transformation of cGMP to its inactive form 5_-GMP.
By inhibiting the degradation of cGMP, PDE5 inhibitors prolong the activity of this cyclic nucleotide second messenger within the cavernous vasculature and smooth musculature, thus potentiating the erectile response. The ability to function sexually helps men define their role and shapes their identity.Loss of erectile function can be devastating. But this psychological factors have only second turn in the ED as the primary cause will be some other causes, leading to it.
It’s estimated that 25 percent of all cases of ED have medication as their underlying cause. But the truth is that Erectile dysfunction(Male infertility) is not an inevitable consequence of aging. It strikes 5 percent of men who are 40 years old, but that number rises to 15 to 25 percent for those age 65 and older. Taken for one hour before planned sexual intercourse, it is effective for a wide range of disorders causing erectile dysfunction. Sildenafil acts by blocking the latter enzyme and as a result increases both the number and duration of erections in men with erectile dysfunction.
This also applies to corpus cavernosum function, where local smooth muscle relaxation, and in turn erection, is mediated predominantly by NO release. This leads to complete filling of the cavernous sinusoids and subsequently to a considerable increase of the intracavernous pressure. The rapid filling of the cavernosal spaces compresses venules resulting in decreased venous outflow, a process often referred to as the corporeal veno-occlusive mechanism. The condition, sometimes called impotence, affects an estimated 15 million to 30 million men in the U.S. In the phase of full rigidity, intracavernous pressure reaches values considerably higher than systemic (systolic) blood pressure.During male sexual arousal, NO is released either at parasympathetic NANC nerve terminals on the cavernous smooth muscle cell or at parasympathetic cholinergic nerve terminals on the endothelial cell lining of the sinusoids. The combination of increased inflow and decreased outflow rapidly raises intracavernosal pressure resulting in progressive penile rigidity and full erection. While the topic was once taboo, awareness has skyrocketed with recent advances in treatment for ED.ED vs. Through membrane-bound G proteins, NO activates guanylate cyclase, which induces cleavage of guanosine triphosphate to 3',5'-cyclic guanosine monophosphate (3',5'-cGMP).The smooth muscle-relaxing effects of NO are mediated by this second messenger (cGMP).
Poor LibidoThere are several forms of male sexual dysfunction, including poor libido and problems with ejaculation. Cyclic GMP activates protein kinase G (PKG), which phosphorylates proteins at the so-called maxi-potassium channels.
This results in an outflow of potassium (K+) ions into the extracellular space with subsequent hyperpolarization, with inhibition or blockade of voltage-dependent calcium (Ca++) channels and therefore a decrease in intracellular Ca++ ion concentrations. ED can be treated at any age.The Mechanics of EDAn erection occurs when blood fills two chambers known as the corpora cavernosa. This causes the penis to expand and stiffen, much like a balloon as it is filled with water.

Other conditions that may cause ED include cardiovascular disease, atherosclerosis (hardening of the arteries), kidney disease, and multiple sclerosis.
Smoking, excessive drinking, and drug abuse may damage the blood vessels and reduce blood flow to the penis. In some cases, the nerve damage is permanent, and the patient will require treatment to achieve an erection. 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.ED and BicyclingResearch suggests avid cyclists suffer more ED than other athletes.
This area between the anus and scrotum contains arteries and nerves vital to sexual arousal.
The doctor will conduct a complete physical exam to uncover signs such as poor circulation or nerve trouble. Measuring testosterone levels can determine whether there is a hormonal imbalance, which is often linked to decreased desire.
A 2010 study suggests ED is a strong predictor of heart attack, stroke, and death from cardiovascular disease.
The researchers say all men diagnosed with ED should be evaluated for cardiovascular disease. Giving up smoking, losing weight, and exercising more often can help by improving blood flow. They're generally taken an hour before sexual activity and should not be used more than once a day.
Cialis can be taken up to 36 hours before sexual activity and also comes in a lower, daily dose.
Drugs approved for this purpose work by widening the blood vessels, causing the penis to become engorged with blood.
Good candidates are typically younger men whose blockage stems from an injury to the crotch or pelvis.
When an erection is desired, the man uses a pump to fill the cylinders with pressurized fluid. A therapist can teach the man and his partner techniques to reduce performance anxiety and improve intimacy. Asian ginseng and ginkgo biloba (seen here) are popular, but there isn't a lot of good research on their effectiveness. An investigation discovered the pills often contain prescription drugs not listed on the label, including the active ingredient in Viagra. Talking openly about ED will help your partner understand the diagnosis and treatment options.

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