Hormones, stress

CRH (Corticotropin releasing hormone) is expressed in the nucleus paraventricularis of the hypothalamus and drives the stress hormone system by activating synthesis and release of corticotropin at the pituitary and in turn corticosteroid from the adrenal cortex. CRH is also expressed at many other brain locations not involved in neuroendocrine regulation, e.g. the prefrontal cortex and the amygdala. Preclinical studies have shown that CRH also coordinates the behavioral adaptation to stress (e.g. anxiety, loss of appetite, decreased sleepiness, autonomic changes, loss of libido). 

In fact, we observed the ability of cationic PO (pi 9.3) to bind with the purified cell walls of this pathogen (Fig. 8, A). This isoform was activated in the infected plants and under the influence of the stress hormone jasmonic acid, both individually and in combination with salicylic acid. 

Chaouloff, F (1993) Physiopharmacological interactions between stress hormones and central serotonergic systems. Brain Res. 18 1-32. 

Several neuropeptides are under current investigation for their role in anxiety disorders. Important neuropeptides include neuropeptide Y (NPY), substance P, and cholecystokinin. NPY appears to have a role in reducing the effect of stress hormones and inhibiting activity of the LC. Both mechanisms may contribute to the anxiolytic properties seen experimentally. Substance P may have anxiolytic and antidepressant properties. This may be due in part to its effects on corticotropin-releasing hormone.21... 

IL-1 (17.5) Monocyte/macrophage, lymphocyte, neutrophil, endothelium, fibroblast keratinocyte Activation of T cells, B cells, natural killer cells, osteoblasts, and endothelium. Induces fever, sleep, anorexia, ACTH release, hepatic acute phase protein synthesis and HSPs. Leads to myocardial depression, hypercoagulability, hypotension/sbock, and death. Simulates production of TNF, IL-6, and IL-8 and stress hormone release. Suppression of cytochrome P-450, thyro-globulin, and lipoprotein synthesis. Procoagulant activity. Antiviral activity. 

Intravenous administration of rTNF induces a disease state that closely resembles septic shock accompananied by tissue damage (M28, T12). TNF induces fever, leukocyte aggregation, hypotension, stress hormone release, lung edema, and hemorrhagic necrosis of various organs (T12). 

Stress Hormones 5.1.1. Hypothalamic-Pituitary-Adrenal Axis... 

In addition to the classical stress hormones already reviewed, several other hormones are augmented in response to stress. Stress-induced prolactin release is one of the most frequently studied examples. There is no doubt about the causal relationship between stress and increased pituitary prolactin release, but the biological meaning is much less clear (G2). This phylogenetically old hormone has been shown to have more than 85 different functions in all vertebrate species. However, besides its role in the induction of maternal lactogenesis, the physiological importance of prolactin is at present not fully established. Experimental and clinical evidence supports the view that prolactin is also an immunoregulating hormone (M44, R18). Prolactin receptors are present on human T and B lymphocytes (R18), and T lymphocytes depend on prolactin for maintenance of immunocompetence (B19). In addition, it has been shown that prolactin is able to influence the devel-... 

The endogenous release of the potent vasoconstrictor neuropeptide Y (NPY) is increased during sepsis and the highest levels are detected in patients with shock (A8). NPY is a 36-amino-acid peptide belonging to the pancreatic polypeptide family of neuroendocrine peptides (T2). It is one of the most abundant peptides present in the brain and is widely expressed by neurons in the central and peripheral nervous systems as well as the adrenal medulla (A3). NPY coexists with norepinephrine in peripheral sympathetic nerves and is released together with norepinephrine (LI9, W14). NPY causes direct vasoconstriction of cerebral, coronary, and mesenteric arteries and also potentiates norepinephrine-induced vasoconstriction in these arterial beds (T8). It appears that vasoconstriction caused by NPY does not counterbalance the vasodilatator effects of substance P in patients with sepsis. The properties of vasodilatation and smooth muscle contraction of substance P are well known (14), but because of the morphological distribution and the neuroendocrine effects a possible stress hormone function for substance P was also advocated (J7). Substance P, which is a potent vasodilatator agent and has an innervation pathway similar to that of NPY, shows a low plasma concentration in septic patients with and without shock (A8). 

Stressful early life events, involving abuse or neglect, can have a life-long influence on the stress response, and lead to elevated levels of allostatic load for the lifespan. Overactivity of the stress hormone axis has been linked to prenatal stress or poor maternal care in rodent models, and this overactivity contributes to increased rates of brain and body aging [39]. 

Thus, the evidence that stress, and the stress hormone corticosterone, may cause changes in hippocampal structure, hippocampal connections, and changes in gene and protein expression, suggest that viable targets of anxiolytic agents are cellular signaling pathways involved in neuroplasticity and the maintenance of cellular resilience. 

The impacts of contaminants on the structure of the immune system can be assessed by examining white blood cell (WBC) numbers and the mass and cellularity of immune organs, although these indicators are usually not as sensitive as measures of immune function. Avian immunotoxicity studies frequently assess total and (or) differential WBC counts [79], and immunosuppression can be indicated by reduced numbers of WBCs or elevated WBC numbers caused by recurrent infections. An elevated heterophil to lymphocyte ratio can indicate altered immune status in response to corticosteroid stress hormones or other factors [78,7 9], Exposure to lead shot or lead acetate has been shown to alter total and (or) differential WBC numbers in Japanese quail (Coturnix coturnix) and mallards [81-83], In western grebes (Aechmophorus occidentalis) from California, concentrations of mercury in the kidney were positively correlated with heterophil... 

Dhabhar, F.S. and McEwen, B.S., Enhancing versus suppressive effects of stress hormones on skin immune function, Proc. Natl. Acad. Sci. USA, 96, 1059, 1999. 

Elenkov, I J. and Chrousos, G.P., Stress hormones, Thl/Th2 patterns, pro/antiinflammatory cytokines and susceptibility to disease, Trends Endocrinol. Metab., 10, 359, 1999. 

Bioavailability of Ca2+ is affected by numerous physiological conditions, including age, sex, genetic make-up, stress, hormonal status, health status, and nutritional habits. In addition to these intrinsic factors, certain dietary components, such as fiber and oxalate, form insoluble complexes with Ca2+ and interfere with its absorption. Another putative culprit in this category is phytic acid. 

McCormick CM, Kehoe P, Mallinson K, Cecchi L, Frye CA. 2002. Neonatal isolation alters stress hormone and meso-limbic dopamine release in juvenile rats. Pharmacol Biochem Behav 73(1) 77-85. 

Stress and stress hormones Anxiety or stress can increase energy expenditure, although the effect is small. It is caused by increased sympathetic activity and hence increased levels of the stress hormones adrenaline and noradrenaline. Injection of these hormones increases oxygen consumption, as does caffeine, which... 

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