It doesn't make any sense to me why blocking the heat receptor (TRPV1) causes heat sensations symptoms in all the clinical trials where TRPV1 antagonists were tried (example: NEO6860 trial).
Can someone pleaaseee explain
TL;DR: Can CGRP antagonists possibly bind to TRPV1 receptors causing people who use cannabinoids to develop Cannabinoid Hyperemesis Syndrome?
Hi all
A recent study (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5758720/) indicates Cannabinoid Hyperemesis Syndrome is caused by excessive and prolonged cannabis use causing CB1 to bind to the TRPV1 receptor and render it inactive. This causes all sorts of gastrointestinal and thermoregulatory issues, and can result in cyclical vomiting that isnβt helped by 5-HT3 anti-emetics. The only thing that helps is hot showers and capsaicin ointment, because for some reason they temporarily knockout the CB1 bound to the receptors.
I am curious if it is feasible that a CGRP antagonist could be blocking TRPV1 receptors, and that would cause a higher incidence of Cannabinoid Hyperemesis Syndrome in people who normally wouldnβt have that issue due to CB1 also binding to that receptor.
Additionally, CGRP is indicated in gallbladder constriction issues (https://www.ncbi.nlm.nih.gov/m/pubmed/9430789/). Iβm curious if there is a CGRP antagonist could cause low ejection fraction in gallbladder.
TIA
In case anyone is clicking just for the title, TRPV1 receptors help us taste spicy food as "hot." I.E. if you eat some Carolina Reaper beef jerky, you'll "taste" it twice.
So... why do we have them 'down there?' What evolutionary advantage does feeling spicy poop offer us? Why out of all of the seemingly random tastes that we can experience 'down there' is spice the only one that really seems to last throughout the entire digestive process?
So TRPV1 is expected to be the receptor for noxious heat stimulus (43 degrees Celcius +) but why do the antagonists show increased heat (not noxious heat just heat) sensations when it was in clinical trials?
TL;DR: Can CGRP antagonists possibly bind to TRPV1 receptors causing people who use cannabinoids to develop Cannabinoid Hyperemesis Syndrome? Can CGRP antagonists cause low gallbladder ejection fraction?
Hi all,
Not a neurobiologist but wanted to talk through and make sure Iβm not linking things that arenβt real. A recent study (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5758720/) indicates Cannabinoid Hyperemesis Syndrome is caused by excessive and prolonged cannabis use causing CB1 to bind to the TRPV1 receptor and render it inactive. This causes all sorts of gastrointestinal and thermoregulatory issues, and can result in cyclical vomiting that isnβt helped by 5-HT3 anti-emetics. The only thing that helps is hot showers and capsaicin ointment, because for some reason they temporarily knockout the CB1 bound to the receptors.
I am curious if it is feasible that a CGRP antagonist could be blocking TRPV1 receptors, and that would cause a higher incidence of Cannabinoid Hyperemesis Syndrome in people who normally wouldnβt have that issue due to CB1 also binding to that receptor.
Additionally, CGRP is indicated in gallbladder constriction issues (https://www.ncbi.nlm.nih.gov/m/pubmed/9430789/). Iβm curious if the CGRP antagonist could cause low ejection fraction in gallbladders
TIA
