Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of LH and FSH in male rats were compared in blood samples collected by decapitation or through permanently implanted aortic cannulae. The hormone levels were higher in the samples taken by decapitation. After cannulation, the gonadotropin levels remained unchanged when sampling occurred only once a day and each rat was bled 1-3 times over a period of 7 days (sample volume 2.3 ml). The hematocrits of these rats decreased from 42% to 34% after two samplings. In another experiment the LH and FSH levels increased when seven samples had been taken during 24 h. In this experiment the blood cells were reinfused into the circulation, and as a result after 5 samples the hematocrit decreased only from 45% to 40%. A drop in food consumption was observed after cannulation. It is suggested that the increase in gonadotropin levels may be due to the acute stress caused by handling during and before decapitation or decrease in gonadotropin levels may be due to the chronic stress caused by the implanted cannula. The frequent bleedings and cell infusions into the cannulated rats may stimulate the secretion of gonadotropins, opposing the effect of chronic stress.
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PMID:The effect of blood sampling on plasma levels of LH and FSH in male rats. 643 50

In conclusion, we have demonstrated that in the primate increased activity of the immune system and the consequent IL-1 release result in the activation of neuropeptides of the adrenal axis, mainly CRF and AVP. These neuropeptides, through a direct effect on the GnRH pulse generator or indirectly through the hypothalamic endogenous opioid peptides, inhibit the GnRH pulse generator. Some of the POMC derivatives, such as alpha-MSH, may antagonize these effects. The consequential decrease in GnRH pulse frequency results in an acute decrease in LH and FSH secretion. This decrease in gonadotropin release may explain the deleterious effects of stress on the menstrual cycle. However, an acute decrease in gonadotropins following activation of the adrenal axis is not observed in the presence of estradiol. Thus, during the menstrual cycle, a relative protection against the deleterious effects of acute stress may exist. How potent this protective mechanism is against repetitive stress is not known.
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PMID:Neuropeptides, the stress response, and the hypothalamo-pituitary-gonadal axis in the female rhesus monkey. 825 5

Chronic stress, understood as a disturbance of the body homeostasis, is partially driven by many hormonal pathways. Prolactine, TSH (Thyrotropin), vasopresin, FSH (Follicle-Stimulating Hormone), LH (Luteinizing Hormone), and GH (Growth Hormone) have been involved in many stress reactions. In acute stress, there are many evidences for the increased both cathecolaminergic and hypothalamic-pituitary-adrenal axis. In chronic conditions, these hyperactivations are controversial and some cases may present a true hypoadrenalism. There is no evidence that treating such androgen/glucocorticoids deficiency may relief chronic pain processes such as fibromyalgia. However, treating somatotroph axis dysfunctions (somatostatin, GH/IGF1 [growth hormone/ insulin-like growth factor-1]) with recombinant GH in carefully seleccioned subgroups of fibromyalgic syndrome, offers us an in-vivo model of the capacity of some hormones to modulate pain.
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PMID:[Stress and chronic pain: An endocrine perspective]. 2179 52

CRH has been implicated as a mediator of stress-induced effects on the hypothalamus-pituitary-gonad axis, acting via CRH receptors in various brain regions. We investigated whether the effects of restraint stress on the secretion of gonadotropins on the morning of proestrus are mediated by the CRH-R1 or CRH-R2 receptors in the oval subdivision of the anterolateral BST, the central amygdala, the locus coeruleus (LC), or the A1 and A2 neuron groups in the medulla. At proestrus morning, rats were injected with antalarmin (a CRH-R1 antagonist), asstressin2-B (a CRH-R2 antagonist) or vehicles. Thirty minutes after the injection, the animals were placed into restraints for 30 min, and blood was sampled for 2 h. At the end of the experiment, the brains were removed for immunofluorescence analyses. Restraint stress increased the levels of FSH and LH. Antalarmin blocked the stress-induced increases in FSH and LH secretion, but astressin2-B only blocked the increase in FSH secretion. LC showed intense stress-induced neuronal activity. FOS/tyrosine-hydroxylase coexpression in LC was reduced by antalarmin, but not astressin2-B. The CRH-R1 receptor, more than CRH-R2 receptor, appears to be essential for the stimulation of the hypothalamus-pituitary-gonad axis by acute stress; this response is likely mediated in part by noradrenergic neurons in the LC. We postulate that the stress-induced facilitation of reproductive function is mediated, at least in part, by CRH action through CRH-R1 on noradrenaline neurons residing in the LC that trigger GnRH discharge and gonadotropin secretion.
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PMID:Divergent roles of the CRH receptors in the control of gonadotropin secretion induced by acute restraint stress at proestrus. 2289 22

Clusterin is a sulfated glycoprotein abundantly expressed in the pituitary gland and hypothalamus of mammals. However, its physiological role in neuroendocrine function is largely unknown. In the present study, we investigated the effects of intracerebroventricular (ICV) administration of clusterin on plasma pituitary hormone levels in normal rats. Single ICV injection of clusterin provoked neurohormonal changes seen under acute stress condition: increased plasma adrenocorticotropic hormone (ACTH), corticosterone, GH and prolactin levels and decreased LH and FSH levels. Consistently, hypothalamic and pituitary clusterin expression levels were upregulated following a restraint stress, suggesting an involvement of endogenous clusterin in stress-induced neurohormonal changes. In the pituitary intermediate lobe, clusterin was coexpressed with proopiomelanocortin (POMC), a precursor of ACTH. Treatment of clusterin in POMC expressing AtT-20 pituitary cells increased basal and corticotropin-releasing hormone (CRH)-stimulated POMC promoter activities and intracellular cAMP levels. Furthermore, clusterin treatment triggered ACTH secretion from AtT-20 cells in a CRH-dependent manner, indicating that increased clusterin under stressful conditions may augment CRH-stimulated ACTH production and release. In summary, hypothalamic and pituitary clusterin may function as a modulator of neurohormonal responses under stressful conditions.
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PMID:Hypothalamic and pituitary clusterin modulates neurohormonal responses to stress. 2408 Aug 98