Concerning the endocrine response, these observations are in agreement with the auxiliary role of vasopressin in the control of the LHPA axis. Continuing interest in the involvement of neuropeptides other than ACTH secretagogues in stress and emerging availability of selective analogues suggests novel possibilities for the use of such agents in pharmacological stress modeling.30,74 Persistent hypercorticalism has been shown to result in deterioration of neuroendocrine circuits that control Inhibitors,research,lifescience,medical the basal activity of the LHPA axis
and its responsiveness to stressful challenges.4 This outcome can be brought about pharmacologically by long-term administration of supraphysiological doses of glucocorticoids. Although this approach is confined to the LHPA axis and manifestation of stress-related symptoms in other systems has not been meticulously Inhibitors,research,lifescience,medical examined, distinct signs of basal hyperactivity and exaggerated endocrine responses to stress persist in this model for {Selleck Anti-cancer Compound Library|Selleck Anticancer Compound Library|Selleck Anti-cancer Compound Library|Selleck Anticancer Compound Library|Selleckchem Anti-cancer Compound Library|Selleckchem Anticancer Compound Library|Selleckchem Anti-cancer Compound Library|Selleckchem Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|Anti-cancer Compound Library|Anticancer Compound Library|buy Anti-cancer Compound Library|Anti-cancer Compound Library ic50|Anti-cancer Compound Library price|Anti-cancer Compound Library cost|Anti-cancer Compound Library solubility dmso|Anti-cancer Compound Library purchase|Anti-cancer Compound Library manufacturer|Anti-cancer Compound Library research buy|Anti-cancer Compound Library order|Anti-cancer Compound Library mouse|Anti-cancer Compound Library chemical structure|Anti-cancer Compound Library mw|Anti-cancer Compound Library molecular weight|Anti-cancer Compound Library datasheet|Anti-cancer Compound Library supplier|Anti-cancer Compound Library in vitro|Anti-cancer Compound Library cell line|Anti-cancer Compound Library concentration|Anti-cancer Compound Library nmr|Anti-cancer Compound Library in vivo|Anti-cancer Compound Library clinical trial|Anti-cancer Compound Library cell assay|Anti-cancer Compound Library screening|Anti-cancer Compound Library high throughput|buy Anticancer Compound Library|Anticancer Compound Library ic50|Anticancer Compound Library price|Anticancer Compound Library cost|Anticancer Compound Library solubility dmso|Anticancer Compound Library purchase|Anticancer Compound Library manufacturer|Anticancer Compound Library research buy|Anticancer Compound Library order|Anticancer Compound Library chemical structure|Anticancer Compound Library datasheet|Anticancer Compound Library supplier|Anticancer Compound Library in vitro|Anticancer Compound Library cell line|Anticancer Compound Library concentration|Anticancer Compound Library clinical trial|Anticancer Compound Library cell assay|Anticancer Compound Library screening|Anticancer Compound Library high throughput|Anti-cancer Compound high throughput screening| several weeks upon
cessation of the glucocorticoid treatment.75 A typical example of pharmacologically induced activation of several stress-reactive systems is represented Inhibitors,research,lifescience,medical by peptide mediators/integrators of the inflammatory and immune responses. The most frequently used agents are tumor necrosis factor a, interleukin-1 and interleukin6, or their sequential releaser, bacterial lipopolysaccharide (LPS). Endotoxinor cytokine-induced effects involve a complex of typical defensive behavioral responses, referred to as “sickness behavior,”
with vagal afferentation playing an essential role.76 Alterations in central and peripheral neurotransmission Inhibitors,research,lifescience,medical largely resemble those evoked by physical and neurogenic stress modalities,77 and activation Inhibitors,research,lifescience,medical of the LHPA axis is a firmly established consequence.78 Suppression of reproductive functions as part of the “sickness behavior,” and in terms of endocrine secretions79 has been demonstrated; it seems that cytokine-mediated disruption of the gonadal axis employs mechanisms which are independent of those involved in the general stress response. The reports on changes in growth hormone and prolactin secretion upon cytokine challenge are second ambivalent. The list of drugs with stressogenic properties becomes considerably longer if LHPA axis activation is considered a solitary symptom of stress. Association of thyreotoxicosis with symptoms of hypercorticalism has prompted experimental studies showing that chronic administration of thyroid hormones leads to activation of the LHPA axis.80 Increased secretion of ACTH and glucocorticoids has been also seen following treatment with cholinomimetics, adenosine and histamine agonists, phosphodiesterase inhibitors, free fatty acids, and a high-fat diet. However, convincing evidence is still lacking that these agents are able to elicit a full-scale stress response.