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getting back to the facts |
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To
recap: statistically, only 10% of men seek help
in dealing with erectile dysfunction (ED). Plus,
it is estimated that, in some degree, ED is
experienced by more than 50% of men over 40. And, in the United States alone,
about
30 million men are victims to ED.
> So, in more detail, how can Tribulus.ext help? |
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Tribulus.ext works in two ways: |
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(1)
Tribulus.ext operates similarly to most popular
pharmaceutical ED products by inhibiting the
enzyme phosphodiesterase-5, medically termed
PDE-5. Inhibiting the function of PDE-5 helps
the smooth muscles in the penis relax and widen,
allowing for a greater amount of blood to enter
this region. Hence facilitating and increasing
the magnitude of the erection.
* As
a side note: Men who do not exhibit any sexual
dysfunction could perform better sexually when
using a nutraceutical with PDE-5 inhibiting
properties.
(2)
Tribulus.ext supports the many hormonal
mechanisms responsible for initiating sexual
drive and enhancing sexual performance. It
raises levels of testosterone, dopamine, and
adrenal hormones responsible for sexual
performance. |
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Below is a Closer Look on the Physiology of
the Erection: |
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Diagram
1: Erection occurs when blood flows into the corpus
cavernosum (CC), which is composed of sinusoids lined by
endothelial cells and smooth muscle cells. At then
onset of an erection, arterioles bringing blood to the
penis and dilate causing the sinusoidal smooth
muscle cells relax, while outflow is limited by pinching
of the subtunical venules and emissary vein, causing the
penis to become erect and rigid. |
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Diagram
2: A key event in penile erection is relaxation of
the CC smooth muscle cells, which is initiated locally
by acetylcholine (Ach) and nitric oxide (NO) as well as
other physiological agents. Ach is generated by
parasympathetic nervous system neurons and NO is
produced by nonadrenergic, noncholinergic (NANC)
neurons, and by hormonal stimulation of endothelial
cells. The net effect is to override sympathetic
nervous tone (alpha stimulation), which causes smooth
muscle cell contraction and maintains the penis in a
flaccid state.
Intracellular molecular events that occur following
exposure of the smooth muscle cells to NO triggers the
conversion of GTP to cyclic GMP (cGMP). This, in turn,
triggers a biochemical cascade that leads to CC smooth
muscle cell relaxation. CC smooth muscle relaxation
depends on the balance of concentrations of cGMP and the
rate cGMP is converted to its inactive state by PDE-5; a
higher concentration of active cGMP equates to CC
smooth muscle relaxation.
Simply,
inhibiting PDE-5 is key to prevent cGMP into its
inactive state. And, as described above, a higher
concentration of cGMP means more blood entering the CC
smooth muscles, therefore allowing for a fuller
erection. |
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