Neuroendocrine mechanisms of stress ulceration: focus on thyrotropin-releasing hormone (TRH).
It is generally accepted that stress ulceration, a multifactorial or pluricausal gastrointestinal disorder, may be the result of mechanistic interrelationships between mucosal, vascular, hormonal and neurogenic factors. The relative importance of each of these independent mechanisms remains unclear. This minireview represents an attempt to interpret many recent studies on certain neurogenic mechanisms and to integrate these observations into the existing body of knowledge. A variety of in vitro techniques and animal models to manipulate actual structures, organ systems, and certain well-defined hormonal influences have been utilized. The peripheral studies have followed, for the most part, the established observation that the stomach is under reciprocal control by sympathetic inhibitory and parasympathetic excitatory autonomic fibers. As a result, several autonomic adrenergic neurotransmitter substances have been found to promote mucosal resistance. Some of these include dopamine, epinephrine, and norepinephrine. Others in contrast, appear to promote vulnerability of the mucosa, and of these, the most well-studied include acetylcholine and histamine.
D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology; D002395:Catecholamines / Q000502:physiology; D006801:Humans; D009419:Nerve Tissue Proteins / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D013276:Stomach Ulcer / Q000209:etiology* / Q000503:physiopathology; D013312:Stress, Physiological / Q000150:complications* / Q000503:physiopathology; D013973:Thyrotropin-Releasing Hormone / Q000502:physiology*
D002395:Catecholamines; D009419:Nerve Tissue Proteins; D018377:Neurotransmitter Agents; D013973:Thyrotropin-Releasing Hormone