How Viagra Works
|
|
Viagra® is one of the best-known drugs of all time:
* Google lists over 17 million Web pages that use the word “Viagra.” For comparison, Google lists only 3.3 million pages containing the word “aspirin” and only 936,000 containing the word “Tylenol.”
* Billions of spam e-mail messages advertise Viagra® every day. There is so much Viagra spam, in fact, that Pfizer (the maker of Viagra) has a page addressing the problem, called Avoid Fake Viagra, prominently listed on Viagra.com.
* Pfizer has spent untold millions of dollars advertising Viagra®, so you see advertisements for the drug constantly on TV.
* Pfizer claims on its Web site that nine Viagra® pills are dispensed every second—nearly 300 million tablets per year.
The name recognition of Viagra® is so good that nearly every adult in America has heard of the drug and can tell you what it does.
What Viagra® does is simple: When it works as intended, Viagra® causes a man who is sexually stimulated to get an erection.
How does Viagra® do that? And why does Viagra® work only if the man is sexually stimulated? For that matter, what causes an erection in the first place? In this article, we’ll answer all of those questions and more.
This is actually a fascinating story—it involves the technology of the human body and the techniques that scientists use to control different parts of the body with drugs. And in the case of Viagra®, the story starts with the technology of the penis…
Physiology of penile erection
The central sensory psychogenic stimuli or penile stimulation or both increase parasympathetic activity, resulting in relaxation of the penile smooth muscle (Saenz de Tejada & Moncada 1996). This phenomenon is mediated by activation of the NO/cGMP pathway and by additional activation of the cAMP pathway, which result in increased blood flow through the penile arteries.
NO exerts a significant impact on the penis, operating as the princial mediator of ED (Burnett 1997). NO is a free radical and therefore a highly reactive and chemically unstable molecule. NO crosses the plasma membrane of cells targeting on the guanylate cyclase enzyme, producing a conformational change in the molecule that increases its activity. Activated guanylate cyclase catalyzes the conversion of guanosine-5``-triphosphate (GTP) to 3`,5`cyclic guanosine monophosphate (cGMP). The accumulation of cGMP sets in motion a cascade of events at the intracellular level which induce a loss of contractile tone of penile smooth muscle and increase of bood flow in cavernous body.
The other pathway for inducing relaxation and erection is mediated by vasoactive intestinal peptide (VIP) (Ehmke et al. 1995). The VIP receptors in the cavernous body are coupled to specific proteins that stimulate the catalytic activity of adenylate cyclase with the formation of cAMP. Endogenous prostanoids participate in the regulation of penile smooth muscle contractility. The receptor that mediates relaxation to PGE is designated ”EP receptor”. The stimulation of beta-adrenergic receptors by catecholamines causes relaxation of the arterial and trabecular smooth muscle. The beta-2 subtype is probably the most important receptor mediating these effects (Dhabuwala et al. 1985). Adrenaline has high affinity for this receptor, whose stimulation partly counteracts the constrictor effects of this catecholamine, which are mediated by alpha-adrenergic receptors.
One of the mechanisms by which cyclic nucleotides induce the relaxation of smooth muscle is through the opening of potassium channels, which hyperpolarize the cell. The activation of potassium channels by PGE1 action, an effect mediated by AMPc, has been demonstrated (Christ et al. 1996).
The termination of erection takes place via increased adrenergic activity, and it has two components: a direct constrictor effect on the smooth muscle mediated by the alpha1- and alpha2-receptors and an indirect effect, whereby the vasodilatator effect of noncholinergic neurotransmitter nerves is inhibited by a prejunctional, alpha2-adrenergic-mediated mechanism (Saenz de Tajada & Moncada 1996).
Physiology: how an erection happens
The creation of an erection is an extremely complicated cascade of events that requires many different things to happen. There are numerous chemical transmitters involved in this including epinephrine, norepinephrine, acetylcholine, prostaglandins and nitric oxide. The exact mechanism by which erection occurs is still unclear but we do know that the neural input from the brain is extremely important. Reflex erections, as seen in people with cord damage such as paraplegics, are often poor erections and not sustainable for prolonged periods of intercourse.
An erection occurs when the nervous system activates a rapid increase in blood flow. The vascular muscle in the spongy area becomes engorged with blood and theoutflow of blood is cut off. An erection can occur as a reflex as we see in spinal cord patients, or can be caused by psychogenic (originating in the mind) stimulation. Numerous sexual stimuli are processed by the brain and transmitted to the penis via the nervous system.
In order to increase the size of an erection, there must be an increase in blood flow and, at the same time, the blood has to be prevented from leaving the penis.
Print Version
Tell-a-Friend comments powered by Disqus
