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In addition to the central nervous system, glutamate receptors have been recently identified in a number of peripheral tissues, including adrenals. Pharmacological evidence indicates that adrenal glutamate receptors may be involved in stress response, particularly in catecholamine release. However, possible stress-induced changes at the level of local receptors themselves have not been evaluated yet. This study was aimed to investigate gene expression of N-methyl-D-aspartate (NMDA) receptor subunits (NR1, NR2A, NR2B) in rat adrenal gland under basal and stress conditions, using RT-PCR. NR1 mRNA was found to be present in the adrenal gland, while mRNAs coding for NR2-type subunits failed to be detected in adrenal tissue. The distribution of NR1 mRNA in rat adrenals showed higher concentrations in the adrenal medulla (228%) compared to those in the cortex. Single stress stimulus (immobilization) induced a significant increase of NR1 gene expression in both medullar (by 25%) and cortical (by 66%) regions of the adrenal gland at 24 h, while no changes were observed at 3 h after the stress exposure. It is possible that delayed rise in adrenal NR1 gene expression following stress exposure represents one of the factors by which stress exerts long-term effects on adrenal function at the molecular level.
We tested whether simulation of postural changes, which occur during public speech test procedures, activates cardiovascular system and stress hormone release that could interfere with the effect of psychosocial stress load. Young healthy male volunteers (n=8) underwent procedure imitating exactly all postural changes present in the psychosocial stress model based on public speech used in this laboratory (namely changes from sitting to standing and repeated sitting). Postural changes were associated with increases in heart rate, blood pressure, plasma concentrations of noradrenaline and aldosterone and elevation in plasma renin activity. In contrast to cardiovascular parameters, adrenocorticotropic hormone, cortisol and adrenaline, the main characteristics of hormonal response during mental stress, were not significantly influenced. The overall magnitude of all observed alterations was much smaller than that seen following mental stress procedures in our previous studies. This study provides evidence that changes in body posture during public speech test procedure influence hemodynamics and endocrine responses in a mild manner. Though this influence may represent a source of unspecific variance, substantial confounding effects on responses to the psychosocial component of the procedure are unlikely. In any case, models combining mental stressors and changes in body posture must be interpreted as complex stress stimuli.
The standardized extract of Ginkgo biloba (EGb 761) was found not only to improve memory and aging associated cognitive deficits but also to exert beneficial effects on mood. An antistress action of the extract has been suggested but not directly proven. The present study was aimed to evaluate the effects of EGb 761 on salivary cortisol and blood pressure responses during stress in healthy young volunteers (n=70) in a double blind placebo controlled design. A stress model involving a combination of static exercise (handgrip) and mental stimuli was used. Single treatment with EGb 761 (120 mg) reduced stress-induced rise in blood pressure without affecting the heart rate. Salivary cortisol responses showed differences with respect to the gender and the time of day of the stress exposure, with the activation only in male subjects in the afternoon. This activation was absent if they were treated with EGb 761. The performance in a short memory test with higher scores achieved by women remained unaffected by EGb 761 treatment. Thus, this study provides evidence that EGb 761 has an inhibitory action on blood pressure and it may influence cortisol release in response to some stress stimuli.
Stress is considered to be a risk factor of several diseases. The following hypotheses were tested: (1) single exposure to an intensive stressor is followed by endothelial stimulation and/or damage to endothelial cells, (2) potential stress-induced endothelial cell damage is reduced by repeated pretreatment with pentoxifylline and (3) pentoxifylline treatment modifies neuroendocrine activation during stress reflected by changes in hypothalamic-pituitary-adrenocortical (HPA) axis function. Rats were treated with saline or pentoxifylline (20 mg/kg, s.c.) once daily for 7 days and then exposed to single immobilization stress for 20 or 120 min. In saline pretreated rats, stress exposure was followed by a rise in endothelaemia, von Willebrand factor concentrations, adrenocorticotropic hormone (ACTH) and corticosterone release, as well as by enhanced gene expression of hypothalamic corticotropin releasing factor (CRH). Stress-induced changes were reduced by pretreatment with pentoxifylline. Significant inhibition was observed in endothelaemia, plasma ACTH and corticosterone concentration in the adrenals. Thus, signs of endothelial injury as well as stress-induced hormone levels were reduced by pretreatment with pentoxifylline, although there is no evidence for a causal relationship. This protective action of pentoxifylline might be of benefit in the prevention and therapy of some stress-related disorders.
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