Aims: 

For a long period it was generally accepted that glucocorticoids released during stress are ulcerogenic hormones. We designed some experimental studies to clarify the validity of the widely held view that the glucocorticoids released during activation of the HPA axis are harmful to the gastric mucosa.

Methods: 

We examined the effect of glucocorticoid deficiency or the glucocorticoid receptor antagonist RU-38486 on stress-induced gastric erosion, parameters of general body homeostasis and local gastric function in rats. Glucocorticoid deficiency was created by different approaches and followed by corticosterone replacement.

Results: 

The data obtained show that the reduction in the stress-induced corticosterone release, or its actions, aggravates stress-caused gastric erosion. It is suggested that an acute increase in corticosterone during stress protects the stomach against stress-induced injury. Accordingly our results various ulcerogenic stimuli (aspirin, indomethacin, ethanol, acetic acid), similar to stress, induce an increase in glucocorticoid production that helps the gastric mucosa to resist against a harmful action of the ulcerogenic stimuli. Glucocorticoids exhibit gastroprotective effect by both maintaining local defensive factors and inhibiting pathogenic elements. The contribution of glucocorticoids to gastroprotection is tightly related with their contribution to general body homeostasis. Glucocorticoids exert gastroprotective actions in co-operation with prostaglandins, nitric oxide and capsaicin-sensitive sensory neurons: their compensatory action is observed when the protective mechanism provided by either of these factors is impaired.

Conclusion: 

The results suggest that glucocorticoids released during acute activation of the HPA axis are naturally occurring gastroprotective factors.

Supported by FNM RAS-2007, RFBR-07-04-00622, OBN RAS-2007.