Hypothalamic-pituitary-adrenocortical axis: the hidden gold in gastric mucosal homeostasis.
ABSTRACT The results overviewed in the present article suggest that glucocorticoids released during acute activation of hypothalamic-pituitary-adrenocortical (HPA) axis are important gastroprotective factors, allowing us to re-evaluate the traditional point of view about their ulcerogenic role. It has been shown that various ulcerogenic stimuli induce an increase in glucocorticoid production that in turn helps the gastric mucosa to resist against a harmful action of ulcerogenic stimuli. Glucocorticoids released in response to mild stress contribute to adaptive gastric cytoprotection. The gastroprotective action of glucocorticoids is accounted for by maintaining the local defensive factors and inhibiting the pathogenic elements. Maintenance of glucose and temperature homeostasis as well as systemic blood pressure by glucocorticoid hormones could be a fundamental of their beneficial action on various gastric targets. Thus, glucocorticoids released during activation of HPA axis may contribute to the gastric mucosal homeostasis through their contribution to general body homeostasis.
- SourceAvailable from: Dóra Zelena[Show abstract] [Hide abstract]
ABSTRACT: In the everyday life, stress is deemed as something unfavorable that may enhance the risk for the development or worsen a disease. However, in its nature, stress is adaptive reaction of the body. Its main characteristic is the activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. Previously, we have shown that activation of the HPA axis plays a gastroprotective role during acute stress. The aim of our study was to clarify the effects of chronic stress and chronically elevated basal corticosterone levels on the gastric ulceration and cardiovascular vulnerability in rats.Methods. Male Wistar rats were repeatedly restrained 60 min daily for 14 days and examined on day 15th. The gastric ulceration was induced by a s.c. injection of indomethacin (35 mg/kg). The cardiovascular vulnerability was examined in urethane-anaesthetized rats in an experimental angina pectoris model (epinephrine, 10 µg/kg, 30 s later phentolamine, 15 mg/kg, both i.v.).Results. We confirmed the development of chronic stress consequences by changes in several somatic parameters (body weight decrease, thymus involution, adrenal gland hypertrophy), and elevated resting corticosterone levels. However, the gastroprotective effect of chronic stress was not manifested and there was no aggravation of indomethacin-induced gastric ulceration, either. In the experimental angina pectoris model, previous chronic stress did not have any profound effect on the blood pressure, heart rate, and electrocardiogram changes.Conclusions. In contrast to the general view on the harmfulness nature of the stress, we were unable to find a harmful effect of chronic stress on the internal diseases (gastric ulceration and angina pectoris). However, its protective effect was also missing among present experimental conditions. Keywords: chronic stress, indomethacin-induced gastric ulceration, experimental angina pectoris.Endocrine regulations 10/2013; 47(4):177-88. DOI:10.4149/endo_2013_04_177
- [Show abstract] [Hide abstract]
ABSTRACT: Glucocorticoid hormones have dual action on the stomach: gastroprotective and ulcerogenic one. The present study was designed to investigate how physiological gastroprotective action of glucocorticoids can be transformed to pathological ulcerogenic effect. Dose- and time-dependent effects of single injection of dexamethasone on indomethacin-induced gastric erosions, corticosterone and blood glucose levels, somatic parameters were investigated in rats. Dexamethasone at the doses of 0.1, 1, 10 mg/kg decreased the gastric erosion area dose dependently in the case of its injection 1 h before indomethacin administration. Gastroprotective action of dexamethasone (at a dose of 1 mg/kg) was also observed in the case of its injection 6 and 12 h before indomethacin. However, the further increase in the time interval caused transformation of gastroprotective action of dexamethasone to ulcerogenic one. Accordingly to the data obtained short-term maintenance of blood glucose level provides the gastroprotective action of dexamethasone, while dexamethasone-induced long-lasting maintenance of blood glucose level accompanied with the signs of catabolic effects may be responsible at least partly for its ulcerogenic effect.Inflammopharmacology 02/2009; 17(1):15-22. DOI:10.1007/s10787-008-8046-3
- [Show abstract] [Hide abstract]
ABSTRACT: It is known that preconditioning stress may attenuate stress-induced gastric injury and that this effect is mediated by prostaglandins. In the present study we investigated the contribution of glucocorticoids to the gastroprotective effect of preconditioning stress. The effects of mild stress on gastric erosion caused by severe stress were compared in rats with normal and deficient corticosterone response to preconditioning mild stress. Mild stress decreased the gastric ulceration caused by severe stress, and this effect was prevented by glucocorticoid deficiency during mild stress. The results suggest that glucocorticoids released during preconditioning mild stress contribute to the gastroprotective effect of this stress.Annals of the New York Academy of Sciences 01/2009; 1148:209-12. DOI:10.1196/annals.1410.005 · 4.31 Impact Factor