The Chemical PE Thread

The effect of relaxin on collagen metabolism in the nonpregnant rat pubic symphysis

The effect of relaxin on collagen metabolism in the nonpregnant rat pubic symphysis: the influence of estrogen and progesterone in regulating relaxin activity

Relaxin administration significantly increased the length (140 +/- 6%) and weight (170 +/- 9%) of the interpubic fibrocartilage…

At the same time, it decreased the total collagen content by 68 +/- 6%, without altering the proportions of collagen types…

Relaxin administered alone reduced the total collagen content by 64 +/- 4% but had no effect on collagen solubility or composition…

Relaxin as a natural agent for vascular health.

Relaxin as a natural agent for vascular health

…RLX has a specific relaxant effect on peripheral and coronary vasculature, exerted by the stimulation of endogenous nitric oxide (NO) generation by cells of the vascular wall, and can induce angiogenesis.

Relaxin regulates MMP expression and promotes satellite cell mobilization during muscle healing…

Relaxin regulates MMP expression and promotes satellite cell mobilization during muscle healing in both young and aged mice

The polypeptide hormone relaxin has been proven to be effective in promoting both the remodeling and regeneration of various tissues, including cardiac muscle.

relaxin promoted myogenic differentiation, migration, and activation of matrix metalloproteinases (MMPs) …

Meanwhile, both angiogenesis and revascularization were increased, while the extended inflammatory reaction was repressed in the relaxin-treated…

Speculation!

Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis.

Follistatin improves skeletal muscle healing after injury and disease through an interaction with muscle regeneration, angiogenesis, and fibrosis

I have heard of links to PE for Follistatin, this link sound an awful like the effect relaxin can have…. its just similar but make you wonder if it works with smooth muscle.

Hey Inuic, have you ever done any reading about inhibiting Myostatin and PE? A few months ago I found a patent applied for by a doctor that pretty much touches on just that. I made a thread about it, but at the time ChempPE wasn’t being talked about as much and it fell by the wayside. I’ll just link to my post, as it already has the relevant info. Probably better than copying/pasting the same thing in here. Curious to hear your thoughts on it, since I noticed a lot of your own research is a little more complicated and development-related.

Myostatin Expression & PE

Can anyone tell me whether or not we actually have reason to believe that changing anything in the penis other than the dimensions of the CC cahnges the size of the penis when erect?

It seems a lot of these things might increase the number of blood vessels and mass of smooth muscle. But since they are inside the CC, then increasing these things would not change a person’s BPEL and EG.

What do you guys think? Maybe someone with weak erections would benefit from angiogenesis. But not someone with strong erections.

In a nutshell, mechanical stimulation (i.e. intermittent stretch) results in the production and efflux of two prostaglandins, PGE2 and PGF2a. PGE2 increases protein degradation where as PGF2a increases protein synthesis. Muscle hypertrophy is usually achieved by an increase in protein synthesis as well as a proportionately smaller increase in degradation. The simultaneous release of both PGE2 and PGF2a creates this condition.

It is well known that mechanical stretch, without any electrical activity, is sufficient to induce muscle hypertrophy. Recent studies have shown that the mechanism by which mechanical stretch leads to prostaglandin production and ultimately muscle growth, involves G proteins embedded in the cell membrane. These G proteins increase the amount of cyclo-oxygenase, the enzyme responsible for making prostaglandins from arachidonic acid. Skeletal muscle cyclooxygenase generates PGE2 and PGF2 alpha at a ratio approximately equal to one.

If you recall, when a muscle is stretched it not only produces PGF2a, but also PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is how existing muscle cells increase the number of nuclei they contain. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications on growth and development as well as stretch induced hypertrophy.

PGF2a + IGF-1: The ultimate cocktail for localized growth?!

With the advent of PGF2a as a localized anabolic agent along with rhIGF-1 which has also been shown to build muscle where you want it. A brief refresher course on locally injected IGF-1. Non-exercised muscle, when injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 was shown to mimic the effects of physically loading the muscle. Much the same effect PGF2a but by different mechanisms. With local IGF-1 injections there is an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 needed are extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.

Now add PGF2a to the mix and whalla! You can virtually mimic the mechanical stimulus of training. You have PGF2a to accelerate short term protein synthesis by activating ribosomes and/or eIFs and thereby translation, as well as IGF-1 to activate satellite cells to bind and donate additional nuclei to boost the amount of mRNA to be used by the ribosomes. Because the mechanism of action is different, the two compounds should compliment each other delivering results beyond what either one alone could produce.

But what makes you believe that increasing muscle content would result in a larger erect penis? I would think the only thing that would result in a larger erect penis would be a larger CC, and the CC is not made of muscle.

Sentil,

The effect is based on some earlier posts about PGF2a and PGE1 and PGE2. It showed they have effects on not just MUSCLE, but more importantly SMOOTH MUSCLE. The CC is made of smooth muscle, and if you weaken the Tunica and expand the smooth muscle via hypertrophy, and angigenesis,\myogenesis. So the idea is that PGF2a has effect both on smooth muscle and normal muscle, and it indicated in the penis patent and used with success. These are clues as to why and what else may synergize its known effects, namely IGF-1 and the like.

inuic

Nice doc shows much of whats been tried on PD…Which can give clues to Tunica delimiters. Weakend the outer balloon of the tunica by breaking down the collagen then expand the smooth muscle via cell multipliers and vein multipliers.

Inuic

Sentil,

Grow more veins inside Tunica makes it fatter, give more bud sites for new veins to grow via Chemical PE and its various methods. Use PGE-1 to keep a constant internal pressure hence blowing up the balloon at full max for extended periods of time. Weaken the balloon via what breaks down collagen and its more like a thin condom. Now when the internal pressure is great it extends past the former limit of the balloon and the new veins that grow have a place to grow into as the Tunica limit is breached. Hence the penis expands. Weaken the ligament that delimits length via things like Relaxin, and then when you hang, jelq, pull or what have you it has more effect. You still do manual PE this stuff just syngergizes and compliments whats going on bio-physiologically when you do so. and some may simulate whats going on via manual PE alone. Think of it as like fertalizer for the penis, plants dont need it to grow, but it sure can help if done right. Its worked for my, I also did 2 priapus shots with good effect in a short time.

Inuic.

On the patent he says that topical gel or creams could very well work to deliver the chemicals mentioned . DMSO ?
“Because of the penises location and the large ratio between the size of the body relative to the penis, the preferred embodiment for these agents would be topical creams, gels, patches or local injections in combination with some form of mechanical mechanism also applied to the penis.”

inuic,
don’t you think that once the tunica is weakened , normal erections can make smooth muscle normally develop to accustom the new size,without the need of pge1 and such ?

Also in the patent, when he says traction device he refers to hanging ? extender ? or it doesn’t matter?

Transdermal application of verapamil gel to the penile shaft fails to infiltrate the tunica albuginea - PubMed

This study’s conclusion

"These data indicate that applying transdermal verapamil gel to the penile shaft results in a small amount of systemic absorption but the gel does not infiltrate the tunica albuginea. Based on these findings the use of transdermal verapamil for Peyronie’s disease has no scientific basis."

I always found that study to be interesting, since I’d like to think Verapamil is a worthwhile topical compound. The results are unfortunate, but I find this excerpt from the aforementioned 2011 patent add-on to be interesting:
”The inventor treated several patients’ Peyronies’s Disease and penis enlargement patients with the recommended dosing and frequency for direct Verapamil injections into the penis and into plaque with no observable effect. However, the inventor discovered that certain doses of Calcium Channel Blockers and Calmodulin Blockers, when applied topically, infused continuously, or applied intermittently at a higher frequency than was recommended in the medical literature improved their clinical efficacy.”

So what he essentially alleges, is that you have to use much more than the typical dose, with more frequent application for it to work as it should on the tunica. Not sure where I stand on the whole thing. I’m glad that apparently he found a way to properly utilize such a compound, but the results of both studies leave me feeling somewhat conflicted.

I am skeptic that you can inject anything significant into the tunica. Do you know how thin TA is?