I found this online:http://www.asiatour.com/how_non_subscriber.htm
looks like maybe the idea is to REDUCE norepinephrine. so the gnarly side effects are when you just have too nor stashed in there making it impossible to get an erection and with time you can reduce the amount of it being produced because you are forcing it to circulate rather than hit the receptors and that tells your brain over time to stop making so much. explains a lot about how the sides went away for me and i could get it up fine but then i didnt attribute it to any yohimbe and stopped it. i think im gonna run a 90 day cycle of yohimbe without stopping at all
A large number of neurologically active pharmaceuticals actually do not affect nerve cells themselves but rather the neurotransmitters in between. Yohimbine is such a pharmaceutical. It blocks the receptor sites for the neurotransmitter norepinephrine. More specifically, yohimbine blocks presynaptic alpha-2-adrenergic receptors. By thus interfering with the sympathetic nervous system, the parasympathetic nervous pathway will prevail in controlling a large number of involuntary bodily functions. Peripheral vasoconstriction (a tightening of blood vessels in the extremities) will be hindered, resulting in more blood flow to those extremities. Among the extremities that benefit from this condition is the male erectile organ. Other symptoms of the parasympathetic nervous system being in charge are the increased salivation as well as the increased digestive activity usually noticed when on yohimbine.
Adrenergic blockade can be effected not just by yohimbine but a considerable number of other pharmaceutical agents as well. And those other pharmaceutical agents do not work as aphrodisiacs or medication against erectile dysfunction. Actually, most adrenergic blockage drugs, such as so-called beta-blockers are known to impair sexual function.
To evaluate the effect of the adrenergic blockage caused by yohimbine, we have to be aware of the differentiation among adrenergic receptors. Four different kinds of receptors have been identified: alpha-1, alpha-2, beta-1, and beta-2. They all are binding sites for the adrenal hormone / neurotransmitter epinephrine. All except for beta-2 receptors are also docking sites for norepinephrine. As the adrenal hormones are practically the same for all receptors, the differentiation is effected by the different receptors.
Heart function and blood pressure are more closely correlated to beta-receptors than to alpha-receptors. Your typical medication for high blood pressure is a beta-blocker.
Beta-blockers are known to cause erectile dysfunction, and the reason is probably the same that answers why yohimbine can cause tachycardia (an abnormally fast heart beat). If epinephrine and norepinephrine are artificially prevented from docking at beta receptors (or alpha-2 receptors), this will result in elevated plasma levels of norepinephrine and epinephrine. The hormone / neurotransmitter will then exhibit an increased tendency to bind to those receptor sites that have not been blocked.
Therefore, it is reasonable to assume that in the case of beta-blockers, there will be an increased pressure on alpha-receptors to accommodate the circulating epinephrine and norepinephrine. Alpha-2 receptors have a major function in erections in that epinephrine and norepinephrine have to be evicted from alpha-2 receptors in order for erections to occur. However, the presence of higher plasma levels of epinephrine and norepinephrine (because of a lack of possibility to dock on beta receptors) will make this more difficult to achieve. Therefore, while beta-blockers cause a decrease in blood pressure and slow down the heart, the adrenergic effect on some peripheral organs, including erectile tissue, is increased. Therefore, beta-blockers have a tendency to cause erectile dysfunction.
Like beta-blockers, alpha-blockers such as yohimbine will cause an increase in plasma levels of the adrenal hormones / neurotransmitters epinephrine and norepinephrine. And if the epinephrine and norepinephrine cannot dock at alpha-2 receptors, there will be an increased tendency to dock at beta-1, beta-2, and alpha-1 receptors. This can lead to hypertension and tachycardia (an abnormally fast heartbeat).
Most of the literature on yohimbine recommends daily use, in order to keep unwanted side effects like nervousness and insomnia at bay. The rationale for such a recommendation is derived from basic facts of the endocrine system.
Practically all hormones have the effect of inhibiting their own production, usually via negative feedback carried through blood plasma to the hypothalamus-pituitary axis. The adrenal hormones / neurotransmitters epinephrine and norepinephrine are no exception.
The hypothalamus measures plasma levels of epinephrine and norepinephrine (as well as plasma levels of most other hormones from the adrenals or other glands); if plasma levels are high, no action is taken; if plasma levels are low, the hypothalamus releases Corticotropin-releasing hormone. Corticotropin-releasing hormone then stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH, corticotropin). Corticotropin then stimulates the adrenals to secret adrenal hormones.The few physicians who do subscribe yohimbine in the age of Viagra usually tell their patients that problems such as restlessness and insomnia subside after several days into a yohimbine cycle. The following could explain what happens.
On the first days of yohimbine ingestion, plasma levels of epinephrine and norepinephrine are artificially high. They remain high until either the alpha-2 adrenergic blockage has been removed (thus again allowing dockage at these receptors, or until elevated plasma epinephrine and norepinephrine will have been dealt with by the liver. As the hypothalamus definitely senses elevated epinephrine and norepinephrine plasma levels, there will, during the first days on a yohimbine cycle, likely be no release of corticotropin-releasing hormone by the hypothalamus, and therefore no release of corticotropin by the pituitary, and thus no additional release of norepinephrine and epinephrine by the adrenal medulla.
Therefore, when into a yohimbine cycle, it is reasonable to assume that the release of epinephrine and norepinephrine will be down-regulated by the hypothalamus … but only with continuous use.
Apart from presynaptic alpha-2-adrenergic receptor blockade, there may be other elements that contribute to the sexuality and erection enhancing power of yohimbine, though presynaptic alpha-2-adrenergic receptor blockade is probably the most relevant element. It has been noted that yohimbine has an anti-diuretic action, probably via the release of the posterior pituitary hormone vasopressin or even via anti-diuretic hormone (ADH). Vasopressin is also available as pharmaceutical product, and as such, it is sometimes used for its sexually stimulating effect. One can assume that the probable release of vasopressin contributes to the sexually stimulating effect of yohimbine. Yohimbine also has an effect on MAO inhibition (covered in another article).