Vagus substance

Choline was isolated from ox bile in 1849 by Strecker. During 1900 to 1920, observations led to interest in the vasodepressor properties of the esters of choline, and in the 1920s it was shown that acetylcholine was presumably the "vagus-substance." The nutritional importance of choline was recognized in the 1930s, when it was found that choline would prevent fatty infiltration of the Hver in rats. Subsequent observations showed that choline deficiency could produce cirrhosis (1) or hemorrhagic kidneys (2) in experimental animals under various conditions. 

Vagusstoff, m. vagus substance, acetylcholine or (2.Vaguasto F) thiamine. 

Substance P is a member of a group of polypeptides known as neurokinins or tachykinins. It is thought to be the primary neurotransmitter for the transfer of sensory information from the periphery to the spinal cord and brain. Substance P as well as neurokinin NKX receptors has been detected in vagal afferent neurons in the area postrema, nucleus tractus solitarius and dorsal motor nucleus of the vagus. Substance P has been shown to increase the firing rate of neurons in the area postrema and nucleus tractus solitarius and to produce retching when applied directly to these areas in animal studies. 

Acetylcholine (ACh) has been known as a neurotransmitter since the mid-1920s. In fact, the demonstration that acetylcholine is the Vagusstoff ( vagus-substance ) released from the vagus nerve to modulate heart function was the first proof for the chemical mediation of nerve impulses (Loewi and Navratil, 1926). In the peripheral nervous system, ACh is found as the neurotransmitter in the autonomic ganglia, the parasympathetic postganglionic synapse, and the neuromuscular endplate. 

The second heart began to beat faster, as had the first, suggesting that some chemical substance was in the fluid and was affecting the heart rate. The experiment indicated that the vagus nerve conveys messages from the brain to the heart by releasing a chemical or chemicals. 

We have already discussed the co-occurrence of small amine and peptide neurotransmitters their release is normally Ca + dependent, and they operate through signal transmission. They are also capable of regulating each other s release and even the synthesis, clustering, and affinity of receptors. Neuroendocrine cells are capable of producing more than one peptide, and thus an amine-peptide as well as a peptide-peptide combination is possible. It is known, for instance, that the vagus nerve contains substance P, vasointestinal peptide, enkephalin, cholecystokinin, and somatostatin— peptides with a hybrid combination of neural and hormonal communication properties. 

Cocaine and other local anesthetics abolish not only the sensation of pain, but other special sensations, if they are suitably applied. Here also there is some selection. In the skin, they paralyze first the vasoconstrictor reaction, then progressively the sensations of cold, warmth, touch, tickling, pressure, pain, and joint sense. In the nose, they abolish the olfactory sense. On the tongue, they destroy the taste for bitter substances but have less effect on sweet and sour taste and none on salty taste. When cocaine is applied to the appropriate nerves, it is found that the centrifugal vagus fibers are paralyzed before the centripetal, vasoconstrictor fibers before vasodilator, bronchial constrictors before the dilators, etc. (Sollmann, 1944). 

Fick (65), in 1873, reported that 4-6 mg. of sparteine injected into the lymph sac of a frog sloAved the heart rate to that of normal and that the ventricular systole was less strong. An antivagal action was indicated in the observation that sparteine prevented the cardiac arrest evoked by the cholinergic substance (muscarine) and caused the vagus nerve to become inexcitable by electrical stimulus. 

The pharmacodynamic action of the nicotine derivatives, such as the a- and a -aminonicotines and a- and a -acetylaminonicotine, was studied by Mednikian (80). The respiratory stimulation which these substances provoke is less pronounced than that produced by nicotine but is more durable. As for the acetylated derivatives, this action is not preceded by an initial respiratory arrest which many other substances in the nicotine group presented. These substances act on the chemoceptors of the carotid body, on the respiratory center itself, and on the intrapulmonary endings of the vagus. 

The full expression of this phenotypic switch in nodose ganglion neurons requires intact vagus nerves, but if allergen reached the systemic circulation in sufficient quantities, it could also stimulate substance P synthesis by local activation of vagal ganglionic mast cells (Chuaychoo et al. 2005). 

These results indicated the involvement of the presynaptic cholinergic and/or substance P neurons, where release of the corresponding neurotransmitter stimulated in turn postsynaptic and/or substance P receptors localized on smooth muscles [13, 15, 39, 65, 66]. Activation of these receptors results in muscle contraction. Morphine is also able to inhibit S-HT mediated contraction suggesting that opiate receptors inhibit the 5-HT4-stimulated acetylcholine release [15]. Much less is known about the localization of S-HT -Rs in myenteric nervous of human and other species. In vivo, h-HT -R agonists are clearly prokinetic in both human and dog [44, 67]. In rat, 5-HT4-RS have also been described on vagus nerves in which they trigger depolarization [68]. 

Gamse, R., Lembeck, F., and Cuello, A. C., 1979ft, Substance P in the vagus nerve immunochemical and immunohistochemical evidence for axoplasmic transport, Naunyn-Schmiedeberg s Arch. Pharmacol. 306 37-44. 

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