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Yohimbine blocks alpha-2 and alpha-1 adrenergic receptors, increasing adrenaline and dopamine and decreasing serotonin levels.
In low doses yohimbine will antagonize alpha2 adrenergic receptors, leading to increased blood flow to the genital area, where blocking the presynaptic alpha2 receptors will lead to an increase in both nitric oxide & noradrenaline release. Blocking alpha-2 adrenoceptors increases blood pressure, releases insulin, and decreases blood sugar levels.
In low doses yohimbine will antagonize alpha2 adrenergic receptors without much CNS stimulation, leading to increased blood flow to the genital area, where blocking the presynaptic alpha2 receptors will lead to an increase in both nitric oxide & noradrenaline release in the Corpus cavernosum. Blocking alpha-2 adrenoceptors increases blood pressure, releases insulin, and decreases blood sugar levels.
Yohimbine also, however, interacts with alpha1 adrenergic receptors, albeit with lower affinity, therefore, at higher doses an α1 blockade can occur and overwhelm the effects of the α2 blockade, making it difficult to predict the response, (alpha1 antagonism reduces blood pressure and overall CNS stimulation) and it will also influence other receptors.
In very high doses yohimbine will also antagonize alpha1-receptors, making it difficult to predict the response, (alpha1 antagonism reduces blood pressure and overall CNS stimulation) and it will also influence other receptors which it only has moderate affinity to, such as 5HT2A, which is one possible explanation for it's ability to induce hallucinations at very high dosages.
Yohimbine behaves as an antagonist at dopamine D2 and D3 receptors, serotonin 5-HT1B, 5-HT1D, 5-HT2A, and 5-HT2B receptors, and as a partial agonist at 5-HT1A.<ref>Agonist and antagonist actions of yohimbine as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors. Significance for the modulation of frontocortical monoaminergic transmission and depressive states. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/10611634</ref>
Because beta2-adrenergic stimulation by the increased levels of adrenaline/noradrenaline also increase insulin release, yohimbine should in theory be taken on an empty stomach if fat loss is the goal, as circulating insulin has a direct inhibitory effect on lipolysis.
Yohimbine hydrochloride (also known as quebrachine) is a naturally-occurringstimulant substance of the tryptamine class derived from the bark of the African tree Pausinystalia johimbe. Yohimbine is the major active constituent of the bark, with the active ingredient being yohimbine hydrochloride. It is commonly used as a fat-burning compound or for to treatment of erectile dysfunction.
Yohimbine is a drug used in veterinary medicine to reverse the effects of xylazine in dogs and deer. It is used as a research reagent. In the US it is prescribed, but now rarely, for erectile dysfunction in men.
Yohimbine is an indole alkaloid molecule of the tryptamine chemical class.
Pharmacology
In low doses yohimbine will antagonize alpha2 adrenergic receptors, leading to increased blood flow to the genital area, where blocking the presynaptic alpha2 receptors will lead to an increase in both nitric oxide & noradrenaline release. Blocking alpha-2 adrenoceptors increases blood pressure, releases insulin, and decreases blood sugar levels.
Yohimbine also, however, interacts with alpha1 adrenergic receptors, albeit with lower affinity, therefore, at higher doses an α1 blockade can occur and overwhelm the effects of the α2 blockade, making it difficult to predict the response, (alpha1 antagonism reduces blood pressure and overall CNS stimulation) and it will also influence other receptors.
Yohimbine behaves as an antagonist at dopamine D2 and D3 receptors, serotonin 5-HT1B, 5-HT1D, 5-HT2A, and 5-HT2B receptors, and as a partial agonist at 5-HT1A.[1]
Subjective effects
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWikicontributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
Physical effects
Stimulation - Stimulation is especially noticeable once you begin an activity that increase adrenaline output, such as training.
There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:
Warning:Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
↑Agonist and antagonist actions of yohimbine as compared to fluparoxan at alpha(2)-adrenergic receptors (AR)s, serotonin (5-HT)(1A), 5-HT(1B), 5-HT(1D) and dopamine D(2) and D(3) receptors. Significance for the modulation of frontocortical monoaminergic transmission and depressive states. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/10611634
↑Evidence for activation of both adrenergic and cholinergic nervous pathways by yohimbine, an alpha 2-adrenoceptor antagonist. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/7557820
↑Differential effects of noradrenergic drugs on anxiety and arousal in healthy volunteers with high and low anxiety. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/9004342
