Talk:Yohimbine: Difference between revisions

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==Pharmacology==

~~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~~.

==Subjective effects==

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*'''[[Effect::Wakefulness]]'''

*'''[[Effect::Cognitive dysphoria]]'''

*'''[[Effect::Emotion enhancement]]'''

}}

@@ Line 11: / Line 11: @@
 ==Pharmacology==
-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.
 ==Subjective effects==
@@ Line 50: / Line 48: @@
 *'''[[Effect::Wakefulness]]'''
 *'''[[Effect::Cognitive dysphoria]]'''
+*'''[[Effect::Emotion enhancement]]'''
 }}
 }}