Does THC bind to ace2 receptors?
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| Papers (10) | Insight |
|---|---|
41 Citations | Thus, immunomodulation induced by THC may be related to receptor effects as well as unrelated to such receptors. |
| 7 These data show that THC causes vasorelaxation through activation of K+ channels and inhibition of Ca2+ channels, and this involves non‐CB1, non‐TRPV1 but G‐protein‐coupled receptors. | |
| In addition, in the effect of the exocannabinoid THC and the endocannabinoid 2-AG, non-CB(1), probably CB(2)-like receptors are also involved. | |
19 Citations | Docking studies suggest that THC(an), although nonaromatic, has a CB(1) receptor binding affinity similar to that of natural THC. |
936 Citations | Consequently, ACE2 receptors limit several detrimental effects resulting from binding of angiotensin II to AT1 receptors, which include vasoconstriction, enhanced inflammation and thrombosis. |
| THC could bind to FA2 and FA7 sites, as substantiated by docking simulations; nevertheless, the observed allosteric effect(s) suggests that the primary binding site of THC is the FA2 cleft that positively modulates heme affinity. | |
22 Citations | We hypothesized that release of anandamide by activation of D2 receptors was responsible for the observed augmentation of THC discrimination. |
| These results show that THC selectively acts at CB1 receptors to reduce neuronal activation in response to emetic stimuli in specific regions of the dorsal vagal complex. | |
| Exogenous activation of these receptors by THC could therefore alter EC levels. | |
| The results of our study clearly demonstrate that both proteins serve as receptors independently of ACE2 and that there is a minimal level of synergy between DC/L-SIGN and ACE2. |