Stress, Neuropeptides and Gastric Mucosa.

Exposure of the organism to a hostile stimulus results in a series of coordinated reactions that aim to avoid the aversive effect and maintain or restore homeostasis of the organism. In response to noxious stimuli corticotropin-releasing factor (CRF), the primary mediator of stress responses is released from the paraventricular nucleus resulting in activation of the hypothalamic-pituitary-adrenocortical axis and coordination of the endocrine, autonomic, behavioral and immune responses to stress. Several other neuropeptides, released in a coordinated way are also involved in the regulation of the stress response. However, besides the development of adaptive physiological, beneficial reactions, pathological, non-desired somatic and psychic responses can also develop, among others: gastric mucosal damage, erosion and ulceration. The mechanism of stress-related gastric mucosal injury is not fully understood; both mucosal injurious and protective mechanisms are activated in response to stress. Decreased mucosal circulation due to redistribution of blood flow from the visceral region toward the vital organs seems to be the primary mechanism of gastric mucosal damage. Mucosal hypoperfusion can result in mucosal ischemia, free radical formation and gastric hypomotiliy. On the other hand, several stressrelated neuropeptides, such as CRF, SP, N/OFQ, opioids, oxytocin and prolactin have been reported to inhibit the stress- and other ulcerogenic stimulus-induced mucosal lesions independently on their effect on other stressrelated symptoms. Consequently, neuropeptides released during stress, besides their numerous physiological and pathophysiological functions, may initiate adaptive mechanisms as well as counteract the stress-induced gastric mucosal injury.