In the central nervous system, nitric oxide is produced enzymatically in postsynaptic structures in response to activation of excitatory amino acid receptors. It then diffuses out to act on neighbouring cellular elements, probably presynaptic nerve endings and astrocyte (glial) processes. Being of such a small size NO is freely diffusible across membranes. That is it does not react with receptors but diffuses into adjacent cells. Because it is so liable NO cannot be stored by conventional means nor inactivated after synaptic release. Its local biosynthesis constitutes the only means for regulating NO levels, hence NOS is one of the most regulated enzymes in biology. Thus the compartmentalization of NOS appears to be crucial for its functionality by providing local NO levels.
The molecule possesses a small dipole moment because of the similar electronegativity of oxygen and nitrogen, making it essentially hydrophobic, that is it's not soluble in water. Its reactivity is due to the unpaired electron in the outer valence orbital of its oxygen constituent. NO is not to be confused with laughing gas or Nitrous Oxide for NO has one extra electron than Nitrous oxide, and turns to nitrogen dioxide on contact with oxygen. NO is a short-lived chemical transmitter, that is almost unreactive as free radical compared to other oxygen radicals. Indeed, NO decays within 6-10 seconds after its synthesis as it interacts with oxygen and superoxide and quickly turned into nitrates and nitrites, or is quickly bound by the iron in hemoglobin and binds with the iron in enzymes also.
In the body, nitric oxide is synthesized from arginine and oxygen by the enzyme nitric oxide synthase (NOS) and requires the presence of calcium for its production. NOS synthesizes NO depending on the availability of L-arginine, which is supplied mainly from glial cells. The uptake of arginine into neurons is controlled by non-NMDA glutamate receptors. Studies demonstrate that white matter glial cells exhibit a large repertoire of neurotransmitter responses linked to Ca++ signalling and that these receptor systems are differentially distributed on sub-populations of glial cells.
NOS is mainly found in the hypothalamus which is the
controller of enzyme excretion, and controls the release of oxytocin
and vasopressin. In the adrenal gland, NOS is highly concentrated in a
web of neurons that stimlate adrenal cells to make adrenaline. NOS is
prominent in fibers and terminals in the posterior pituitary gland but
its function has not yet been established. It is also
found in the intestine, cerebral cortex, and the endothelial layer of
the blood vessels. NO participates in the release of
Gonadotropin-releasing hormone (GnRH) from the hypothalamus. Oxytocin
stimulates the release of luteinizing hormone-releasing hormone (LHRH)
by releasing nitricoxide. The sleep hormone melatonin
reduces NOS
activity in the hypothalamus of rats. For this reason melatonin might
be able to be used to reduce the intenstiy of kundalini activity; it
might also offer some free radical protection as well.
NO has many roles in the cardiovascular system as it is a blood vessel dilator, it thins the blood, reduces platelet stickness, is involved in blood coagulation and wound healing and is associated with the hearts function. The endothelium (inner lining) of blood vessels uses nitric oxide to signal the surrounding smooth muscle to relax, thus dilating the artery and increasing blood flow. NO and its associated release of vasopressin is obviously a major factor in the phenomena of heart expansions during an awakening. It has been shown that hemoglobin is a major transport vehicle for NO in blood.
NO is a major signal transduction molecule in vertebrates and serves as a neurotransmitter in the CNS and the GI tract and may be involved in memory and learning. Unlike most other neurotransmitters that only transmit information from a presynaptic to a postsynaptic neuron, the small nitric oxide molecule can diffuse all over and can thereby act on several nearby neurons, even on those not connected by a synapse. It is thought that this process may be involved in memory through the maintenance of long-term potentiation, or long-lasting strengthening of the connection between two nerve cells. The physiological role of nNOS in mechanisms such as long term potentiation has been shown to involve retrograde transport (diffusion) of NO synthesized in post synaptic neurons across the synaptic cleft into synapses, where it stimulated guanyl cyclase.
Guanylyl cyclase is the enzyme that catalyzes the formation of the messenger cyclic GMP (cGMP) from GTP. It has been established that cGMP plays a role in the relaxation of smooth muscle, the inhibition of platelet aggregation and participates in signal transduction within the nervous system. Moreover, cGMP is involved in the regulation of the water and electrolyte balance as well as in the metabolism of the bone. cGMP is also involved in retinal phototransduction--that is the conversion of a light signal received by a nerve receptor, to an electrical signal transmitted to the brain. Since cGMP is activated by nitric oxide (NO) and peptide hormones and concentrations of both these arise during an awakening, this might help explain transcendental vision, that is the radical increase in visual acuity and sensory perception in general. NO increase in cGMP in retinal photransduction might explain the light shining from the eyes of those who are awakened.
It is cGMP that signals the smooth muscles surrounding the arteries of the penis to relax and allow more blood to flow into the penis. NOS neurons are prominent in penile tissue, and the pelvic plexus, establishing that NO is the transmitter of these nerves which regulate penile erection.
It is interesting that Nitric Oxide fuels both erections and possibly the Inner-conjunction (10,000 orgs) up the spine, because Eastern traditions talk about men ejaculating up their spines. That is they turn the ecstatic energy around so that NO ignites the central channel of the spine rather than being lost in the ejaculation of sperm.
Human Growth Hormone (HGH) is a polypeptide hormone secreted by the anterior pituitary gland that regulates tissue growth, cellular repair, energy levels, fat loss, and muscle growth. Most of the substances that increase NO production also increase HGH. Thus many aphrodisiacs, sexual performance enhancers and HGH supplements will help sustain an awakening by preventing the depletion of NO metabolism. Supporting both HGH and NO production keeps the nervous system in a hyperactivated metamorphic condition.
Prolonged activation of glutamate receptors stimulates eNOS; NMDA receptor activation can increase levels of nitric oxide and hydroxyl radicals.
NO in combo with glutamate makes for radical excitability in the nervous system, for special extreme events like fight, flight, *censored*, birth, death...and the inner-conjunction (10,000 orgs up the spine). It operates as a neurotransmitter, vasodilator, and heart expander, so it is key to increasing blood supply to heart and brain to "feed" the awakening, and is one of the main neurotransmitters involved in the extreme kundalini events and strange symptoms like tingling, gravity warping and kriyas.
As a free radical NO enables white blood cells (macrophages) to kill tumor cells and bacteria. NO is also involved in apoptosis (programmed cell death), DNA breakage and mutation. Thus it is undoubtedly involved in the catabolic breakdown of the body especially during the die-off. The highly liable NO might also be one of the methods by which connective tissue in the body is "released" by kundalini, thus dissolving the old body armor structure.
NO AND NEUROTOXICITY
While NO mediates normal synaptic transmission, excess levels of NO may be neurotoxic. One theory proposes that in the presence of high levels of glutamate, nitric oxide producing neurons behave more like macrophages, releasing lethal amounts of nitric oxide. The neurotoxic effects of NO include depressing glycolysis, DNA damage, depletion of NADH and ATP. The formation of NO is implicated in cell death (apoptosis) through DNA damage, suppressed mitochondrial respiration, leading to energy depletion. Neurons are particularly sensitive to impaired mitochondrial ATP synthesis capacity, because neurons depend almost exclusively on the oxidative degradation of glucose and ketone bodies. The cells energy molecule ATP is used by ion selective pumps to maintain the proper ion gradients, for action potential generation in the nerves and neurotransmitter release in presynaptic membranes.
If we maintain a high intensity of metamorphic fire we will simultaneously have to work towards preventing neuron death by glutamate and NO neurotoxicity. That is we must take antioxidants to prevent free radical and crosslinking damage to cell membranes and DNA. In particular mitochondrial tissue needs to be protected to preserve energy generation. Thus on the one hand we make sure the fire doesn't run out of fuel, or we would plunge into one of the forms of Dark Night, and we simultaneously protect our tissues from the very metamorphic fire we are feeding. In this way we should be able to manage a sustained accelerated evolution and heightened creativity and productivity.
The fatigue that accompanies acute heart expansion is probably primarily due to NO interfering with cellular respiration. While providing an intense burst of neurological activity NO must then lead to exhaustion and energy depletion. NO as an inhibitory effect on oxidative phosphorylation by blocking the electron transport chain and controlling the levels of citrate in the Krebs cycle essentially blocking the oxidative degradation of acetyl-CoA.
Evidence has accumulated for a number of years that glutamate released in excess, acting via NMDA receptors, mediates neurotoxicity in stroke, Alzheimer's and Huntington's diseases. Because glutamate, via NMDA receptors, stimulates NO formation, one might expect excess NMDA receptor stimulation to destroy Nitric Oxide Synthase (NOS) neurons. Surprisingly, NOS neurons are resistant to NMDA neurotoxicity. If NMDA stimulates NOS neurons to make NO, but these cells are themselves resistant to neurotoxicity, could the released NO damage other cells? Exposure of cerebral cortical cultures to NMDA kills 60-90% of neurons, with NOS-diaphorase cells being undamaged. Why are NOS neurons resistant to NMDA toxicity? Presumably, NO is never released in the interior of NOS cells, which accordingly are resistant to NO damage. Glutamate receptors are selective for calcium ions; larger amounts of NO can force the calcium channels to fire more rapidly which can lead to apoptosis or programmed cell death. (See Glutamate)
The body's antioxidant superoxide dismutase prevents the conversion of nitric oxide to peroxynitrite forming hydrogen peroxide. Nitrite reductase not only prolongs the effective 'life time' of NO, but also reduces the concentration of its highly reactive secondary metabolites: Peroxynitrite, hydrogen peroxide, and dinitrotrioxide all have been linked to cell death (apoptosis) through protein nitration and increased mutagenesis. Acute neural toxicity is linked to the overproduction of the secondary NO metabolite peroxynitrite, which inhibits respiratory enzymes and also damages DNA by covalent bond formation to DNA and removal of bases. In glial cells the stimulation of NOS activity causes significant damage to the mitochondrial activities of neighboring neurons. Both a NOS inhibitor and interferon-/§ and antioxidants exhibit neuroprotective properties because they limit the formation of highly reactive nitrogen containing radicals.
NO regulates the function, growth, death and survival of many immune and inflammatory cell types. Mast Cells and their potent chemical mediators are known to initiate and modulate a number of important inflammatory cascades. In Multiple Sclerosis besides T-Lymphocytes and Macrophages it is found that Mast Cells also are indicated in central and peripheral nervous system demyelination.Mast Cells surround blood vessels in the brain, are juxtaposed to neurons. Mast Cells (activated by Myelin Basic Protein), have been shown to secrete vasoactive and inflammatory mediators in response to neuropeptides and direct nerve stimulation and can participate in the regulation of the Blood-Brain Barrier permeability, as well as in myelin destruction.
Kidney failure patients suffer from neurological complications and a
recent study shows how free radicals and NO interact to produce
oxidative stress that helps produce this nerve damage. A powerful
antioxidant (des-methyl-tirilizad) was found to serve some protection
from brain dysfunction during kidney failure. Research results directly
demonstrate that vasopressin stimulates NO release via the endothelial
V1 receptor in the rat kidney.
Septic Shock of the White Death
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 Death 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 Death that tends to
follow the radical peak influx kundalini surges.
http://bja.oxfordjournals.org/cgi/content/full/86/4/578
Another factor that may be involved in the “shock” condition after
extreme kundalini events, is the possible interference with the energy
generation mechanisms in the mitochondria. Mitochondrial DNA is more
susceptible to damage from 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.
“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 mitochondrial
failure is the mitochondrial permeability transition, which both
uncouples oxidative phosphorylation and accelerates ATP hydrolysis.
Interventions that block this pH-dependent phenomenon protect against
onset of cell death.” The Mitochondrial Permeability Transition in Toxic, Hypoxic and Reperfusion Injury, John J. Lemasters et al.
NO AND THE INNER-CONJUNCTION
My present understanding of the metabolization of spiritual alchemy is that we both have to feed the nitric oxide pathways, and preserve the organism from the consequent free radical storm that it creates; note that a lot of the guru types die of cancer. Thus it is highly amusing that for our evolution we need to take aphrodisiacs and antioxidants. How is that for a cosmic joke. I am not sure about the benefit of prolonging an awakening, however, if we can gain higher homeostasis and adapt well to these periods of spiritual acceleration, it stands to reason that we should be able to evolve further in one lifetime by doing so. Logically we should aim for a longer duration burn with less downtime (burnout) by supporting and protecting.
So the ironies of ironies is that the ultimate YES is fueled by NO! In looking for the mechanism of the Inner-conjunction I knew it was probably connected with the ionization of the Cerebrospinal Fluid (CSF), calcium ions and nitric oxide (NO). What I found pretty much convinced me that I had discovered the key to the Inner-conjunction and explained many of the more extreme symptoms of the hyper-aroused peak.
The hyper-activation of the CNS during the height of an awakening would increase the calcium ion (Ca2+) content of the CSF. This in turn leads to the liberation of NO, otherwise known as endothelium-derived relaxing factor (EDRF), which then could defuse into the central channel of the spinal column, since it is the most permeating substance in the body.
The high concentration of NO in the spinal channel during the Inner-conjunction would explain the complete loss of ego and self-sense, the loss of motor control (paralysis), the loss of time-sense and the appearance of Witness consciousness coupled with the experience of Emptiness or Infinity. So we have an ultimate condition that constitutes the total cessation of the mind (daily consensus-rational consciousness)--that is a transcendence of the mind under circumstances of amplified consciousness, not a descent into unconsciousness through anaesthetization of the Mind.
Since NO is a vasodilator and smooth muscle relaxer, this explains the radical relaxation of the autonomic neuromuscular system during these peak "up" phases; this we experience as extreme bliss and love. It also explains the tremendous heart expansions and the sensations of gravity warping. Other vasodilators that may be implicated in this process of somatic "opening" and heart expansion are acetylcholine and vasopressin.
NOS neurons occur in the myenteric plexus that feeds the muscles of the intestinal wall and throughout the gastrointestinal pathway thus NO was found to be a neurotransmitter governing peristalsis. During certain phases of kundalini activity NO dominant chemistry could also explain the digestive dysfunction that occurs when the blissful kundalini is passing directly through the nerves of the GI tract.
The extra nitric oxide present during an Inner-conjunction is probably why men get erections
at this time. And for women, the increased NO and oxytocin is no doubt
the dominant chemistry behind the uterine contractions that last for
the duration of the particular form of Inner-conjunction that I call
Sex with Eros. What makes this event different than a normal
Inner-conjunction is that along with the "10,000 Orgs" up the spine,
there is a continuous spontaneous super-orgasm of the vagina and uterus
lasting around half an hour. Men also
experience a corresponding "sexual" event, which traditionally they
talk about the sense of ejaculating up the spine (which of cause is a
physical impossiblity). These sexually charged inner conjunctions are
more extreme and pleasurable than any normal sex.
Directly following an Inner-conjunction the body looks like it has been fried or electrocuted; probably due to the fact that NO is a free radical gas. The body is so electrically charged that one's hair sticks out. Plus the irises of the eyes are lit from within by an internal light. This is perhaps due to free electrons or photons generated within super-charged proteins (see quote by Stuart Hameroff). It might also be due to extra cGMP from the radical NO metabolism of the inner-conjunction, for cGMP is involved in retinal phototransduction. This heightened flow of electrons through the interiors of protein molecules could be the source behind the luminous glow (aura, halo, aureola) of spiritually lit individuals. When kundalini and bliss is up, there will always be this concomitant glow to the skin.
The following day there is a shift into a massive contraction and autonomic shock (White Death), that is the opposite chemistry of the hyper-arousal and opening. It stands to reason that if we are radically fired up by a free radical gas, that we would "fall back down" in need of some serious R&R.
Obviously the validity of this theory will have to be confirmed by research, but there is the slight problem of finding someone in an Inner-conjunction while in a kundalini research lab. Inner-conjunctions are spontaneous and only last half an hour so in order to study them they will have to be induced, and induced ones will no doubt be different from the real thing. But NO in general should increase for the duration of an awakening, though this might be hard to detect.
NITRIC OXIDE AND SEX
During sexual arousal the brain sends impulses down the spinal cord to the nerves that serve the sex organs. This triggers the production of NO to be released from endothelium in response to acetylcholine and other vasodilators, which causes vasodilation and engorgement. As I mentioned before nitric oxide mediates the formation of cGMP by glutamate stimulation and cGMP signals the smooth muscles surrounding the arteries of the penis to relax and allow blood to flow into the penis. Interference with the signaling of these messenger enzymes can lead to erectile dysfunction. There is some indication that nitric oxide may also function as a sex-enhancing neurotransmitter. I consider NO to be key in amplifying nerve impulses on glutamate nerves, and probably is involved in the functioning of the entire hypothalamus-pituitary-adrenal axis...considering that NO metabolism occurs in all these three areas.
When luteinizing hormone (LH) levels are increased, the natural production of testosterone also increases, as does the sex drive. Opioid neurons are an important inhibitory brake that restrains the secretion of LH. NO is a mediator of glutamate effects in the hypothalamus, meaning that opioid inhibition is mediated on glutamate neurons that are upstream of NO neurons. What this means is that there is an opioid-glutamate-nitric oxide connection in the regulation of testosterone and sex drive. There is also some indication that nitric oxide may also function as a sex-enhancing neurotransmitter.
Viagra (sildenafil citrate) reduces impotency by enhancing the effects of the neurotransmitter nitric oxide (NO), and maintaining higher levels of the enzyme cGMP, the two key factors in penile erection. Viagra does this by selectively inhibiting the enzymes that destroy cGMP, leading to elevated cGMP levels.
It stands to reason that kundalini is centered in sex chemistry, but I didn't know how far until I cottoned onto Nitric Oxide. Close encounters of the sexual kind can kick off a full blown awakening even without actual sex or relationship; thus I suspect that taking a supplemental sexual empowerment protocol will kick off an awakening in of itself. It might add to the intensity if one was ready to pop, but perhaps would not pop one of its own accord. It also reveals why sex and spirituality so often mix in the Guru-student relationship.
"As Conrad describes it, proteins and nucleic acids are extremely complicated nonlinear systems, each with tens of thousands of electrons, protons and neutrons (Conrad, 1996). Some intra-protein electrons are very delocalized and are now known to tunnel long distances through hydrogen bond pathways. Electron delocalization also occurs in surface electrons (which cannot closely follow any specific nuclei) and in aromatic (electron resonance) ring structures in amino acids tyrosine, phenylalanine, tryptophan and histidine. These comprise water-free "hydrophobic pockets" within protein interiors, precisely where general anesthetics act (apparently by limiting electron delocalizability). Conrad observes that significantly delocalized electrons which accelerate relative to their nuclei must then absorb and emit photons whose frequencies cannot be precisely accounted for by the rotational and vibrational transitions of the nuclei. Conrad's model of quantum protein computing argues that superposition of electron states contributes to interference effects that "jiggle the nuclei," in particular the hydrogen bonds, and thereby open up new pathways of conformational self-organization. Parallelism of the electronic wave function is thereby converted to a speedup of protein conformational dynamical function. " ~ Stuart Hameroff
back to Hormones
Continue to Healthy Hormonal Foundation