Research results directly demonstrate that vasopressin stimulates NO release via
the endothelial V1 receptor in the rat kidney.
sePsis oF tHe WHite sHocK
iNO production is a stress response and can lead to either tissue injury because
of its radical chemistry, or be cytoprotective, protecting cells from damage by
destroying pathogenic microorganisms first. The free radicals, however, cannot
discriminate pathogenic DNA from host DNA and overstimulation of iNOS
therefore induces cell and tissue damage, sometimes leading to a fatal development
(septic shock) in the course of bacterial infections. Macrophages produce nitric
oxide in order to kill invading bacteria. Under certain conditions, this can backfire.
Sepsis infection is caused by excess production of nitric oxide by macrophages,
leading to widening of blood vessels, which lowers blood pressure during sepsis.
The autonomic shock of the White Shock could be related to high
plasma concentrations of tetrahydrobiopterin and nitrate, which temporarily
overwhelm the processing capacity of the kidneys. Nitric oxide synthase (NOS)
requires tetrahydrobiopterin for its activity. In sepsis, changes in circulating
tetrahydrobiopterin concentrations precede increases in nitrate. Nitric oxide
is synthesized from L-arginine by the action of nitric oxide synthase and NOS
enzymes require tetrahydrobiopterin for their catalytic activity. Nitric oxide is
important in the maintenance of vasodilator tone and arterial pressure and it has
been suggested that cytokine-mediated circulatory shock is caused by activation of
the inducible isoform (type II) of NOS.2.
Increased production of nitric oxide in response to activation of the type II
isoform of NOS to cytokines has been suggested to be responsible for the hypotension
of septic shock. In patients with weak kidneys (renal failure), both nitrate and
tetrahydrobiopterin concentrations tended to be higher...suggesting that those with
strong kidneys who can adequately process the metabolites through their renal system
may not go through the septic shock or White Shock that tends to follow the radical
peak influx kundalini surges. Besides tumor necrosis factor (TNF), other cytokines
involved in the development of septic shock include interleukin-1B and interferon-y.
http://bja.oxfordjournals.org/cgi/content/full/86/4/578
Another factor that may be involved in the “septic shock” condition after
extreme kundalini events, is the possible interference with the energy generation
mechanisms in the mitochondria by a rapid increase in free radicals. Mitochondrial
DNA is more susceptible to damage from free radicals, toxic chemicals and heavy
metals than DNA in the nuclei of cells. And when mitochondria malfunction
this can lead to a significant drop in energy production. Loss of ATP would mean
less energy for removing toxins and feeding cells, leading to a sudden noxious
overload of toxicity. Putting the organism out of order until the antioxidant and
detoxification mechanisms can rally to deal with the toxic burden.
“Multiple mechanisms contribute to cell injury after hypoxia, ischemia/reperfusion
and toxic chemicals, but a common final pathway leading to acute cellular necrosis
may be ATP depletion after mitochondrial failure. One important mechanism causing