Substance P and Oxygen:
Substance P and oxygen are two of the most fundamental compounds necessary for proper function of the body. Substance P is present in most tissues in the body, and perhaps the best way to view it is as the most primitive sensory system in the body. As such, all other sensory systems are built on top of it, so when its levels go awry, so do other sensory systems (like endocrine, glucose, etc.).
Jaw misalignment causes substance P levels to become elevated throughout the entire body. Excess levels of substance P causes all sensory neurons to become hyper sensitized, hence causing a loss in homeostasis, and subsequently a wide spectrum of medical disorders.
What is little known is that substance P directly influences oxygen levels (see abstract below). Substance P is known to be the primary regulator of the oxygen sensor component of the carotid body. This has the potential in selected cases to seriously impact oxygen levels in all tissues, and most importantly in critical brain cells. I n addition, substance P is a major mediator of inflammation.
Substance P has also been shown to have the ability to significantly increase mitochondrial activity level. This is important in a number of illnesses: cancer, neurodegenerative disorders, autism, etc. (see abstract below). These are major new insights supportive of the suspected link between dental orthopedic defects and cancer.
Peptides. 1989 Sep-Oct;10(5):1003-6.
Substance P and mitochondrial oxygen consumption: evidence for a direct intracellular role for the peptide.
Department of Medicine, Case Western Reserve University, Cleveland, OH 44106.
Substance P (SP), a member of the tachykinin group of peptides, has been shown to augment the sensory discharge of the carotid body, an oxygen sensing chemoreceptor. In this study we present evidence that the excitatory effect of SP, in part, could arise from a direct effect of the peptide on mitochondrial oxidative phosphorylation. Measurement of the partition coefficient of SP showed that the peptide has a relatively high apolar partition, which could be consistent with its distribution across lipid bilayers and in intracellular organelles. In addition, the effects of three concentrations of SP were tested on oxygen consumption of mitochondria isolated from rat hearts. The results showed that while the lower concentration of the peptide (0.5 microM) did not affect O2 consumption, higher concentrations, i.e., 1 and 2 microM, enhanced the rate of state 4 respiration by 52 and 64%, respectively. The rate of state 3 respiration, on the other hand, was unaltered with 0.5 and 1 microM, and was only slightly decreased with 2 microM of the peptide. The ADP:O ratio was unaffected by any concentrations of SP tested. The peptide-induced effect on state 4 respiration was even more pronounced with glutamate as a respiratory substrate and in presence of K+ in the medium. These results indicate that SP, in addition to its more accepted role as a neurotransmitter or modulator in the carotid body, may elicit intracellular response by interfering directly with oxidative phosphorylation.