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The Catecolamine Surge Induced by the Spike Protein
The Spike Protein's agonist relationship with nAChR receptors
The deleterious effects of the Spike Protein can be summed up by Sympathetic Overdrive and Catecolamine Surges. My most recent post details how the Spike Protein induces chronic Sympathetic Overdrive, which I believe is the cause of Long COVID.
I believe I have now determined how the Spike Protein is inducing the Catecolamine Surge, indepently of cardiac manifestations, such as Myocarditis.
The Spike Protein is a nAChR agonist.
The S fragment exerts a dual effect, acting as a low-efficacy agonist and a non-competitive inhibitor. It activates the α7 nAChR, in line with our previous molecular dynamics simulations showing favorable binding of this accessible region of the S protein to the nAChR agonist binding pocket.
A Functional Interaction Between the SARS-CoV-2 Spike Protein and the Human α7 Nicotinic Receptor
This very relationship is what, I believe, is inducing the Catecolamine Surges which, in tandem with its activation of Sympathetic Overdrive, is causing the recent rise in Sudden Cardiac Deaths.
Stimulation of brain nAChRs can induce elevation of plasma catecholamines through brain iNOS‐derived NO‐mediated protein S‐nitrosylation in rats.
Stimulation of brain nicotinic acetylcholine receptors activates adrenomedullary outflow via brain inducible NO synthase‐mediated S‐nitrosylation
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