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  • BDD Moderators: Keif’ Richards

Post GABAergic use vasoconstriction?

Renz Envy

Bluelighter
Joined
Sep 29, 2010
Messages
3,337
I remember reading somewhere that after a depressant is used, your body goes into rebound and constricts blood vessels rather than dilating them like it was doing previously.

Does this hold any merit?

Substances I'm concerned with are: Alcohol, GHB, benzos.
 
Perhaps this is the reason why your extremities become numb and tingly during benzo withdrawal? That makes sense, and coincides with my own experiences with benzos.

Taking an 81mg Aspirin might help you get through vasoconstriction and subsequent increased stroke risk, as it modifies the platelet abilites of blood and allows it to flow better through constricted blood vessels.
 
I dunno, it seems like all GABA-ergics seem to have a rebound of some kind that is very stimulant like. Usually in a negative way.
 
Well, GABA is the inhibitory mechanism of the brain, kind of like the brakes or the "speed governor" some cars come with, making sure we don't speed out of control. When we are hungry, tired, anxious, or in GABA-ergic withdrawal, the lack of GABA doesn't inhibit the brain properly, and it speeds out of control in a negative way.

This is why GABA-ergic use in a non-anxious individual (one who has normal GABA inhibitory processes) causes them to feel numbed, stupid, and slow, the side effects of inhibiting anxiety through inhibiting (slowing down) the rest of the brain.
 
I have never heard of selective GABAergics like benzos having any vasodilatory effect, or any effect on smooth muscle contraction whatsoever.

The mechanism of EtOH-induced vasodilation is distinct from its action as a positive allosteric modulator of the GABAAR. It is likely due to direct interactions with specific ion-channels such as TRPV1, as well as alterations in the NO-dependent pathways.

http://www.ncbi.nlm.nih.gov/pubmed/17888011

http://www.ncbi.nlm.nih.gov/pubmed/14764441
 
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