Now that we known how nitric oxide functions in erectile function, we can evaluate 1,3-DMAA as an anti-erectile agent through norepinephrine (NE). The theory essentially lies in its potentially antagonistic effect on nitric oxide generation, and norepinephrine both inhibits nitric oxide generation and causes smooth muscle contraction in the corpus cavernosum (again, the scientific name for penis, and recall that contraction is bad for erectile function). Since we know that in the corpus cavernosum we are primarily dealing with alpha-adrenergic receptors as well as acetylcholine receptors (AChR), we must assume that 1,3-DMAA affects either one or both. Inevitably, it is related to both, since both ACh and NE play roles in concert in a biological process called “crosstalk”: ACh release inhibits NE release, therein preventing smooth muscle contraction, where, one more time for clarity, smooth muscle contraction is bad for erectile function. (7) Since 1,3-DMAA appears to displace NE as well as inhibit NE transport back into neurons, therein “inactivating” it, it appears to be doing so and causing/exacerbating erectile dysfunction in some users.
Fonte: Primordialperformance
Fonte: Primordialperformance
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