Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Holzer, P.
Neural emergency system in the stomach.
GASTROENTEROLOGY 1998 114: 823-839.
Doi: 10.1016/S0016-5085(98)70597-9
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PubMed
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- Führende Autor*innen der Med Uni Graz
- Holzer Peter
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- Abstract:
- The maintenance of gastric mucosal integrity depends on the rapid alarm of protective mechanisms in the face of pending injury. Afferent neurons of extrinsic origin constitute an emergency system that is called into operation when the gastric mucosa is endangered by acid and other noxious chemicals. The function of these chemoceptive afferents can be manipulated selectively and explored with the excitotoxin capsaicin. Most of the homeostatic actions of capsaicin-sensitive afferents are brought about by peptides released from their peripheral endings in the gastric wall. When stimulated, chemoceptive afferents enhance gastric blood flow and activate hyperemia-dependent and hyperemia-independent mechanisms of protection and repair. In the rodent stomach, these local regulatory roles of sensory neurons are mediated by calcitonin gene-related peptide acting via calcitonin gene-related peptide 1 receptors and neurokinin A acting via neurokinin 2 receptors, with both peptides using nitric oxide as their common messenger. In addition, capsaicin-sensitive neurons form the afferent arc of autonomic reflexes that control secretory and motor functions of the stomach. The pathophysiological potential of the neural emergency system is best portrayed by the gastric hyperemic response to acid backdiffusion, which is signaled by afferent nerve fibers. This mechanism limits damage to the surface of the mucosa and creates favorable conditions for rapid restitution and healing of the wounded mucosa.
- Find related publications in this database (using NLM MeSH Indexing)
- Animals -
- Calcitonin Gene-Related Peptide - physiology
- Capillary Permeability - physiology
- Gastric Mucosa - blood supply
- Humans - blood supply
- Hyperemia - etiology
- Neurons, Afferent - physiology
- Nitric Oxide - physiology
- Research Support, Non-U.S. Gov't - physiology
- Tachykinins - physiology
- Vasodilation - physiology