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Found an interesting drug: Lomerizine and serotonin-induced contraction


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What do you guys think of this?

 

I don't know how much different it is from other calcium channel blockers. It just that it acts on 5HT2a receptors, antagonizes them right? From what I have heard agonising and antagonising of 5HT2a receptors both downregulates these receptors..

 

And a very interesting thing - in wiki it says "serotonin-induced contraction of the basilar artery, which can lead to migraines."

If serotonin can contract the basilar artery, maybe.. since people with HPPD seem to be somehow oversensetive to drugs (many of those people anyway), could the agonisation of serotonin receptors by psychodelics/other drugs, cause some constriction of some blood vessels, seriously restricting the blood flow and doing something to our brain? Ischemia, dysreguletion of something, anything.

 

As I said many times before - I did scintigraphy examination of the brain which shows focal hypoperfusions in two places.. (those responsible for cognition and language etc). Could that be caused by the "serotonin-induced contraction"?

It's like.. if any of the drug did restrict the blood flow - the restriction stayed until months/years later. Is that possible?

 

 

more about the drug itself:

https://en.wikipedia.org/wiki/Lomerizine :

 

Lomerizine (INN) (also known as KB-2796) is a diphenylpiperazine class L-type and T-type calcium channel blocker.[1] This drug is currently used clinically for the treatment of migraines, while also being used experimentally for the treatment of glaucoma and optic nerve injury.

 

Mechanism of Action

Lomerizine works as a calcium antagonist[3] by blocking voltage-dependent calcium channels.[4] A study using [3H]Nitrendipine showed that lomerizine allosterically inhibits binding in calcium channels at a site different than the 1,4 dihydropyridine binding site.[5] However, its antimigraine effects are believed to be due not to the blocking of calcium channels, but to the antagonizing effects of lomerizine on the 5HT2A receptor. The drug was shown to competitively inhibit binding of [3H]spiperone to 5-HT2A receptors, inhibiting the 5-HT driven release of Ca2+. Lomerizine treatment of 5-HT2A expressing cells led to the inhibition of Ca2+ release in response to 5-HT, while Ca2+ release in response to ATP was unaffected.[6] By preventing the release of Ca2+, lomerizine prevents serotonin-induced contraction of the basilar artery, which can lead to migraines.

Lomerizine has also been shown to possess neuroprotective effects, specifically in the case of retinal damage. Doses of .03 mg/kg given intravenously as a pretreatment were shown to prevent glutamate-induced neurotoxicity, while also providing protection against NMDA-induced and kainate-induced neurotoxicity. Lomerizine was shown to have little affinity for NMDA or kainate receptors, so its protectivity against neurotoxicity in these cases is believed to be due to the blocking of Ca2+ influx through voltage-dependent calcium channels.[7] By blocking these channels and preventing Ca2+ release, lomerizine increases circulation in the optic nerve head. These effects show that lomerizine may prove to be a useful treatment for ischemic retinal diseases, such as glaucoma.[7]

Lomerizine also shows neuroprotective effects against secondary degeneration resulting from injury in retinal ganglion cells. In this case, increased membrane depolarization, in conjunction with the inability of the sodium-calcium exchanger to function due to depleted ATP stores, causes the activation of calcium-dependent signal transduction. These processes lead to cell death through either apoptosis or necrosis.[4] Lomerizine's role in blocking Ca2+ can rescue these cells from death by preventing excitotoxicity. Decreased intracellular calcium also prevents necrosis by decreasing permeability, and apoptotic death is reduced through the reduction of calcium-dependent apoptotic agents.[4]

While some calcium-channel blockers, such as flunarizine, act on the dopaminergic system, lomerizine is ineffective in vivo at inhibiting the release of dopamine. However, it has been observed to weakly inhibit the binding of [3H]spiperone to D2 dopamine receptors in vitro.[8] While researchers are unsure of the reason for this difference, one hypothesis is that the doses administered cannot reach a high enough concentration in the brain to affect D2 receptors.[8]

 

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there is a natural way to heal the body him self the body have the best medicen you just need to find way to

i gues you have to realize there is no medicine that can cure hppd or realy help with no side effect there has been so many years passed there is nobody came with a good medicine or i gues you need to realize this is your home (hppd)

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I've asked my doc to prescribe it but now I'm having some reservations. I suffer from headcahes/migraines and have my whole life. I find things get worse for me after I eat certain foods, after sex, drinking and smoking which are common in people who suffer from vasodilatory headaches. Which means the blood vessels are dilated allowing more blood to flow to the brain inducing the headaches or exasperating them. Lomerizine is a vasodilator so I run the risk of things actually getting worse while taking it. Too bad because I really wanted to try it.

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My doctor has agreed to prescribe me either this or flunarazine so I have to pick one. I know people would really like for me to go for lomerizine and we do need some guinea pigs to try new meds but I gotta look out for my best interest too.

Flunarazine has been proven to work. Although I'm prone to depression especially while coming off lamitrogine it is very intense and I can't risk it getting worse

Lomerizine has never been used for hppd but it does look like it tackles a lot of what we need. How ever it is a vasodilator which I don't think would mix well given the type of headaches I get. Also because it works on the 5h2a receptor is there any risk of it making me trip out? Like it stimulates it and I end up making my hppd worse? And given it messes with serotonin that makes me apprehensive too. I need as much of that shit as possible.

decisions decisions

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The choice is yours, flunarizine has been proven to cause Parkinson's disease as it acts in the dopamine channel, which is why American countries have banned it, but lomerizine acts more on the serotonin channels which is why it in theory should work better for hppd. Like I said the choice is yours but we would all like to know what lomerizine is like as it is the only thing some can get prescribed

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