Smooth Muscle and PE

Another one:

Angiogenetic Signaling through Hypoxia
HMGB1: An Angiogenetic Switch Molecule
Claudia Schlueter*, Holger Weber, Britta Meyer*, Piere Rogalla*, Kerstin Röser, Sven Hauke* and Jörn Bullerdiek*

Immunolocalization of the angiogenetic factor pleiotrophin (PTN) in the growth plate of mice:

Or this:

European Journal of Cardio-Thoracic Surgery, Vol 7, 637-643, Copyright © 1993 by European Association for Cardio-thoracic Surgery

Growth of “new” coronary vascular structures by angiogenetic growth factors
K Schlaudraff, B Schumacher, BU von Specht, R Seitelberger, V Schlosser and R Fasol
Department of Cardiovascular Surgery, University of Freiburg, Germany.

The efficacy of the human angiogenetic heparin-binding growth factor I (HBGF-I) to initiate site-directed growth of new blood vessels from the aorta into the myocardium was studied. First, manipulated Escherichia coli bacteria, which had received the human mRNA-transcript for HBGF I into their genetic material, were cultivated. The growth factor derived was purified using heparin-Sepharose affinity chromatography. The separation and characterization of biologically active alpha- and beta- chains was carried out using high pressure liquid chromatography (HPLC) of dialyzed and lyophilized samples from the heparin-Sepharose column. One microgram HBGF I (alpha-ECGF) was bound to polytetrafluoroethylene (PTFE) sponges, precoated with collagen type I, and implanted between the aorta and the myocardium of the left ventricle in experimental rats. Twelve growth factor implants in the experimental group were compared to six controls receiving uncoated PTFE sponges for 9 weeks. Digitized computed angiography showed new blood vessels between the aorta and the myocardium in 11 of the 12 experimental animals, and retrograde coronary perfusion by these “new” vascular structures could be seen. Histology showed no specific structures in the control group (without HBGF I). In the experimental group (with HBGF I) individual vessels with highly differentiated endothelial and smooth muscle cell layers were evident. Our experiments proved the feasibility of induced, site-directed angiogenesis. It is possible to initiate in vivo growth of new “coronary” vascular structures between the aorta and the myocardium.

From Wikipedia ‘angiogenesis’.

Chemical stimulation
Chemical stimulation of angiogenesis is performed by various angiogenic proteins, including several growth factors.

[Edit] Overview
Stimulator Mechanism
FGF Promotes proliferation & differentiation of endothelial cells, smooth muscle cells, and fibroblasts
VEGF Affects permeability
VEGFR and NRP-1 Integrate survival signals
Ang1 and Tie2 Stabilize vessels
PDGF (BB-homodimer) and PDGFR recruit smooth muscle cells
TGF-β, endoglin and TGF-β receptors ↑extracellular matrix production
MCP-1
Integrins αVβ3, αVβ5 (?[9]) and α5β1 Bind matrix macromolecules and proteinases
VE-cadherin and CD31 endothelial junctional molecules
Ephrin Determine formation of arteries or veins
Plasminogen activators remodels extracellular matrix, releases and activates growth factors
Plasminogen activator inhibitor-1 stabilizes nearby vessels
NOS and COX-2
AC133 regulates angioblast differentiation
Id1/Id3 Regulates endothalial transdifferentiation

I hope you are getting the idea :) .

More from Wikipedia (‘angiogenesis’):

VEGF
VEGF (Vascular Endothelial Growth Factor) has been demonstrated to be a major contributor to angiogenesis, increasing the number of capillaries in a given network. Initial in vitro studies demonstrated that bovine capillary endothelial cells will proliferate and show signs of tube structures upon stimulation by VEGF and bFGF, although the results were more pronounced with VEGF[14]. Upregulation of VEGF is a major component of the physiological response to exercise and it’s role in angiogenesis is suspected to be a possible treatment in vascular injuries[15][16][17][18]. In vitro studies clearly demonstrate that VEGF is a potent stimulator of angiogenesis because in the presence of this growth factor plated endothelial cells will proliferate and migrate, eventually forming tube structures resembling capillaries.[8] VEGF causes a massive signaling cascade in endothelial cells. Binding to VEGF receptor-2 (VEGFR-2) starts a tyrosine kinase signaling cascade that stimulates the production of factors that variously stimulate vessel permeability (eNOS, producting NO), proliferation/survival (bFGF), migration (ICAMs/VCAMs/MMPs) and finally differentiation into mature blood vessels. Mechanically, VEGF is upregulated with muscle contractions as a result of increased blood flow to affected areas. The increased flow also causes a large increase in the mRNA production of VEGF receptors 1 and 2. The increase in receptor production means that muscle contractions could cause upregulation of the signaling cascade relating to angiogenesis. As part of the angiogenic signaling cascade, NO is widely considered to be a major contributor to the angiogenic response because inhibition of NO significantly reduces the effects of angiogenic growth factors. However, inhibition of NO during exercise does not inhibit angiogenesis indicating that there are other factors involved in the angiogenic response.[8]

A very good introduction:

In females there is cyclic angiogenesis in the uterus, would be interesting to explore which physiologic stimulators are working there.

Lets be careful with angiogenetic factors.

Don’t even think about injecting this stuff into your self!!

A problem with the systemic application of angiogenetic factors in man could be that it could could promote cancer.

So: the obligatory warning to everybody interested to become a rapid grower: let’s examine that topic together before starting any kind of HUMAN EXPERIMENTS!!

We are no guinea pigs (and if we decide to, then after understanding the pros and cons, the potential merits and the risk - cancer would certainly be NOT ACCEPTABLE).

This isn’t really following the path of this thread but it is an interesting observation about nocturnal erections. This is a post from my progress report.

Had the same strong night wood last night and kept tabs on my unit every now and then to feel what was going on. The CC chambers are very firm while the CS and glans are not. When I kegal the CC pump from firm to hard but again the CS stays the same. It almost seems like a different type of erection than a sexual one. Again the glans are smaller and more of a pointed triangular shape than they are during a sexually aroused erection.

I also noticed that the night erection can last a long time. They seem to last for hours at times. But when they do go away they disappear very rapidly, like in a matter of seconds not minutes. Sexual “arousal” erections seem to linger for a long time in a semi erect state if nothing comes of them (or from them !). They don’t just vanish.

Maybe I’ll have my camera ready in the bathroom one night and try to capture the elusive small headed nocturnal erection.
Shunga

I think the main limiting factor is the tunica. I think once you expand the tunica, then smooth muscle expansion will be almost automatic, or at least easier.

Its like in bodybuilding. What a lot of the empiracle experiences indicates is that if you expand the capsule (fascia) then its far easier to produce hypertrophy.

So, in my mind it gets back to expanding the tunica…but I think there is a very nice thread already prodding that mystery! :)

I totally agree!

Megalophallus / priapism is an example where the vascular system is producing growth of the tunica.

Translated into practical application?

Could it be that hypoxia is compromising the integrity of the tunica, making it weaker and more easily deranged?

Or do you think the vacular system is generating enough stress to expand a normal tunica?

OR…do you think that its a normal stress generated by the vacular system but over a prolonged period resulting in plastic deformaton of the tunica?

Or a combination of the above?

For retracting stretched flaccid measurement.
So if it contracts,the solution is to soften the penis up again make it compliable to your wishes. Manipulate nature do fowfers. I find that if my flaccid is cord like fowfers soften thing right up again. Penis is less resistant to jelqing. It won’t hurt to have a tall glass of water before you PE. You may have to pee but you can always resume after urinating. Explanation, optimal hydration is needed for successful PE. Stay hydrated!

I like this thread I like to offer a nutritional bent.

Thats because the elastin fibers are destroyed, it seems to work for girth.

This seems like a fantastic way to help those atherosclerosis to get an new lease on life. It may even help those with ED at some point. Certainly something to look forward to.

Looking at the various growth factors used in the process of just angiogenesis, it would seem to put PE firmly in the chemical side of the house. As you mention earlier though, there are risks. The only growth factor that the people on this board have access to is IGF-1LR3. This is a research hormone, although it is used illegally by a large number of body builders, and a few PE’ers. The use of IGF-1 will indeed accelerate any cancer that you may have, although there is no evidence (that I have seen) that it causes cancer. I do conceded that it is possible that it may have a causative effect as no one can say with any degree of certainty what does cause cancer.

I also concede that since using IGF-1 requires an injection into the penis that it will not attract many people. Perhaps the knowledge of what can happen may be of interest to some on the board.

Thank you for all of your hard work on behalf of the members.

Stage