Isn’t it funny sometimes, when you start out trying to do one thing, and you end up doing another?
A lot of science goes that way. The guy who invented post-it notes was supposedly trying to make a stronger adhesive. Teflon was supposed to be a refrigerant. And Viagra? Well, they were trying to make a drug to control blood pressure.
It makes sense if you think about it for a minute. High blood pressure is a problem because it increases pressure in the arteries (duh), which means your heart has to work harder to get the blood everywhere it needs to go. But if you took a drug that made your arteries wider, your heart wouldn’t have to push so hard, problem go bye-bye, yes? More or less.
All right, let’s talk about penises now.
A selection of penises from the Iceland Phallological Museum. Yet another reason to visit Icleand. Photo by Wellington Gray.
A guy gets an erection because blood flows into his penis, then stays there. Most men with erectile dysfunction have a problem with their penises filling up with blood. The arteries don’t open up enough, not enough blood can get in, hence no stiffy.
The body regulates arteries widening and constricting, like it regulates pretty much everything else, by chemical cascades. In this particular case, the brain sends a signal through a nerve cell, which triggers the release of nitric oxide, or NO. This turns on an enzyme called guanylate cyclase, which starts making this stuff called cyclic guanosine monophospate, or cGMP for short.
This cGMP is the Barry White in the equation here. It puts those arteries in the penis at ease, so then they relax and open up. Then, schwing! Blood can get in, dude can pitch a tent, and make some sweet sweet love.
Of course, it’s not great biologically to walk around with a constant boner, so there’s something else floating around to make the cGMP go away. It’s yet another enzyme called phosodiesterase, or PDE. There are a lot of different PDEs in our bodies, but the one that rules in the wanger is PDE 5.
PDE 5’s one job is to break down cGMP. No cGMP, no more blood flowing into the penis, and eventually, no more erection. So here’s the pretty cool part: Viagra works by throwing a wrench in PDE 5’s machinery. It’s also known as 5-[2-ethoxy-5-(4-methylpiperazin-1-ylsulfonyl)phenyl]-1- methyl-3-propyl-1,6-dihydro-7H-pyrazolo[4,3-d]pyrimidin-7-one. It looks like so:
And this is what cGMP looks like. See the resemblance?
So PDE 5 is an enzyme, and those work by kind of a lock-in-key type way. A molecule of a certain shape fits into the enzyme, and then the enzyme does what it will with it. In this case, breaks some bonds so the molecule can’t do its job anymore.
But when is sees Viagra floating around in there, it gets confused. That bit in red there? It fits into PDE 5 exactly the same way that cGMP does. So when there’s a lot of Viagra around, the PDE 5 chews it up, instead of the cGMP. So then cGMP can build up in the penis, which makes sure the arteries are opened up. Barry White persists, and the guy gets a chub. Long live Barry White.
Viagra induced woodies can also last up to four hours. So for those of you who can’t get enough? You’re in luck.
Happy Valentine’s Day.
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For further reading (with diagrams!) I suggest Discovery Health’s How Viagra Works page. For the chemists in the crowd, the original paper by Pfizer is pretty interesting: Terrett et al., Bioorganic & Medicinal Chemistry Letters, Vol. 6, No. 15, pp. 1819-1824, 1996.
Oh and btw: the Icelandic Pallological Museum. You’re welcome.
