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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous reports indicate that the central nucleus of the amygdala (CeA) stimulates adrenocorticotropin and corticosterone secretion, suggesting a role for this region in central hypothalamo-pituitary-adrenocortical (HPA) stress regulation. To evaluate this hypothesis, this study assessed the impact of CeA lesion on the response of hypophysiotrophic paraventricular nucleus (PVN) neurons to acute restraint and chronic unpredictable stress exposure. In contrast to previous reports, CeA lesions did not affect corticosterone or ACTH secretion induced by acute stress. Acute restraint increased PVN corticotropin releasing hormone (CRH) mRNA expression, increased the number of parvocellular PVN neurons expressing the co-secretagogue arginine vasopressin (AVP), and induced cFOS mRNA expression in the parvocellular PVN. However, there was no additional effect of CeA lesion on any measure of PVN activation. Chronic unpredictable stress exposure induced long-term activation of the HPA axis, noted by thymic involution, adrenal hypertrophy and increased PVN CRH mRNA expression. Stress-induced changes in thymus and adrenal weights were not affected by CeA lesion. Further, CeA lesion rats did not differ from controls in post-stress CRH mRNA expression. However, basal CRH mRNA expression was increased in the PVN of CeA rats, suggesting that the CeA plays a role in long-term inhibition of the PVN. The results of these studies are not consistent with the hypothesis that the CeA is necessary for stress-induced pituitary-adrenocortical activation. Rather, this region may play a stressor-specific modulatory role in regulation of HPA function.
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PMID:Hypothalamo-Pituitary-Adrenocortical Regulation Following Lesions of the Central Nucleus of the Amygdala. 978 50

The possibility that adrenocortical activation might alter the pyretic effects of bacterial lipopolysaccharide endotoxin in growing pigs was investigated. In a series of four experiments, animals received increasing doses of porcine adrenocorticotrophic hormone ACTH (1.5, 4.5, 13.5 IU kg-1) or CRH (7 microg kg-1), all of which markedly affected cortisol release. Unexpectedly, these treatments tended to increase body temperature during the early and middle stages of the febrile response, although they did appear to induce an earlier deferscence. These results suggest that acute stress may not modify fever induced by immunological challenge, although a different situation could obtain during chronic stress. Furthermore, a hypothesis of fever regulation is proposed which attempts to reconcile the present findings with those from previous studies in swine.
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PMID:Studies of endotoxin-dependent fever in pre-pubertal pigs following acute activation of the pituitary-adrenocortical axis: towards a new hypothesis of fever regulation. 1020 85

Two groups of beagles, accustomed to spacious group housing, were subjected to social and spatial restriction and studied for manifestations of chronic stress with a time interval of 7 weeks between the groups. The change from outside group housing (the control period) to individual housing in small indoor kennels resulted in sustained decreases in urinary adrenaline/creatinine and noradrenaline/creatinine ratios for the total group. Urinary dopamine/creatinine and noradrenaline/adrenaline ratios were statistically unaffected. Socially and spatially restricted dogs that had experienced pleasant weather during the control period showed (a) increased salivary and urinary cortisol concentrations, (b) a diminished responsiveness of the pituitary-adrenal axis to a sudden sound blast or exogenous CRH, (c) intact plasma ACTH and cortisol suppressions after dexamethasone administration, and (d) increased concanavalin A induced lymphocyte proliferations. When social and spatial restriction was preceded by a control period during which the weather was bad, these physiological responses were either augmented (lymphocyte proliferation), or offset (salivary and urinary cortisol), or directed oppositely (CRH-induced ACTH and cortisol responses). Together with the previously presented behavioral observations, these data suggest that bad weather conditions during spacious outdoor group housing induced early stress that attenuated the negative appraisal of the subsequent period of social and spatial restriction. In comparison to male dogs, bitches showed increased HPA responses to a sound blast or exogenous CRH. Their increased attenuations of the ACTH and cortisol responses to CRH after 5 weeks of restricted housing indicates that bitches are not only more susceptible to acute stress, but also to chronic housing stress. It is concluded that the quality of circumstances preceding a period of affected well-being determines the magnitude and even the direction of the behavioral and physiological stress responses. Basal salivary and urinary cortisol measurements are useful for the assessment of chronic stress, and of poor welfare in dogs. The use of urinary catecholamine, peripheral leucocyte, and lymphocyte proliferation measures requires further investigation.
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PMID:Chronic stress in dogs subjected to social and spatial restriction. II. Hormonal and immunological responses. 1033 50

The cellular organization of the paraventricular nucleus (PVN) is complex and eight distinct regions have been identified by Nissl staining. Three consist of magnocellular neurons and five of parvocellular neurons. Ibotenic acid, a glutamate analogue, is a toxin with neuroexcitatory properties which acts on N-methyl-D-aspartate and metabotropic receptors. Depending on the dose used, ibotenic acid causes extensive damage of parvocellular neurons of the paraventricular nucleus but preserves magnocellular neurons and passage fibers, in contrast to electrolytic lesions, which causes diffuse and nonspecific destruction. We studied the prolactin (PRL) and corticosterone secretion in response to acute stress induced by exposure to the ether, 3 weeks after selective neurotoxic lesion of parvocellular neurons of the paraventricular nucleus by microinjection of ibotenic acid. There was no significant difference in the basal levels of PRL and corticosterone between control and lesioned animals. The plasma PRL increased in the sham and lesioned groups after stress of similar manner. However, the increase in plasma corticosterone in response to stress was significantly higher in lesioned animals. In conclusion, the selective lesion of parvocellular neurons of the PVN did not change basal or stress induced PRL secretion but it caused hypersensitivity of the hypothalamus-pituitary-adrenal axis 3 weeks later, probably by corticotropin releasing hormone (CRH) from hypothalamic areas others than parvocellular neurons of the PVN; hypersensitivity of corticotropes to the secretagogues others than CRH; or hyperresponsiveness of AVP receptors in the adenohypophysis. Furthermore, we cannot rule out a putative inhibitory factor of the hypothalamus-pituitary axis produced by parvocellular neurons of the PVN. This factor modulator of corticotropin secretion could be absent after recuperation of the response of the hypothalamus-pituitary axis to the stress.
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PMID:Prolactin and corticosterone secretion in response to acute stress after paraventricular nucleus lesion by ibotenic acid. 1097 87

The aim of the present investigation was to characterize the baroreflex in weaned 23- to 25-day-old rats when maternal influences were no longer present. The relationship between mean arterial pressure (MAP) and heart rate (HR) was determined during baroreceptor loading with phenylephrine and baroreceptor unloading with sodium nitroprusside in conscious rats, first in the freely moving state and subsequently during acute stress. In unstressed rats, the slope of the relationship between MAP and HR was greater during baroreceptor loading than baroreceptor unloading. Acute stress significantly attenuated the slope of the response to baroreceptor loading but increased the slope of the response to baroreceptor unloading. Pretreatment with intracerebroventricular or intravenous losartan, an AT(1) receptor antagonist, or intracerebroventricular alpha-helical corticotropin-releasing hormone (alpha-hCRH), a receptor antagonist, before the stress significantly reduced the stress-induced attenuation of slope during baroreceptor loading. Hence, young postweaning rats can alter baroreflex function during acute stress in a manner that would favor increases in MAP. Even at this young age, a central action of ANG II and CRH contributes to these stress-induced adaptations.
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PMID:Contribution of central ANG II to acute stress-induced changes in baroreflex function in young rats. 1100 8

The present study investigated the role of mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) in the expression of habituation of the hypothalamic-pituitary-adrenal (HPA) axis response to stress. Male rats were restrained for 1 h per day for six consecutive days. On day 6, 1 h prior to restraint stress, both restraint-naive and repeatedly restrained rats were injected s.c. with either vehicle (propylene glycol) or one of three corticosteroid receptor antagonist treatments: selective MR antagonist (RU28318 or spironolactone), selective GR antagonist (RU40555), or both MR and GR antagonists combined (RU28318 + RU40555). Blood samples were collected for corticosterone measurement at the beginning of stress, during stress, and 1 h after stress termination. Repeated restraint stress produced significant habituation of corticosterone responses. Acute treatment with the combined MR and GR antagonists prevented the expression of habituation. When tested alone, the MR antagonist also blocked the expression of corticosterone-response habituation, whereas the GR antagonist had no effect. Neither the MR, nor the GR antagonists alone, significantly altered the corticosterone response to restraint in rats exposed to restraint for the first time. The final experiment examined the corticosterone response to a corticotropin releasing hormone (CRH, 3 microg/kg i.p.) challenge. Neither previous exposure to restraint or acute pretreatment with the combined MR and GR antagonists (RU28318 + RU40555) altered the corticosterone response to CRH challenge. This result indicates that the expression of habituation and its blockade by corticosteroid receptor antagonists is not a result of altered pituitary-adrenal response to CRH. Overall, this study suggests that MR plays an important role in constraining the HPA axis response to restraint stress in restraint-habituated rats. The dependence of the HPA axis on MR-mediated corticosteroid negative feedback during acute stress may be an important mechanism that helps maximize the expression of stress habituation and thereby minimize exposure of target tissues to corticosteroids in the context of repeated stress.
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PMID:Selective blockade of the mineralocorticoid receptor impairs hypothalamic-pituitary-adrenal axis expression of habituation. 1101 46

1. The role of alpha1-adrenergic receptors on CRH mRNA levels in the PVN was studied in control and stressed rats receiving i.c.v. injections of the alpha1-adrenergic agonist, methoxamine, or the alpha1- antagonist, prazosin. 2. Plasma ACTH increased significantly 60 min and 4 hr after a single injection of methoxamine (100 microg, i.c.v.). No desensitization of this response was observed after repeated injections every 6 hr for 24 hr. Concomitantly, POMC mRNA in the anterior pituitary increased by 25% at 4 hr after a single injection and by 96% after repeated injections. 3. CRH mRNA levels in the PVN increased by 131% after repeated injections for 24 hr, but were unchanged 4 hr after a single injection. Central alpha-adrenergic blockade with prazosin did not prevent the increases in CRH mRNA following 4 hr of acute stress, but significantly reduced the increases observed 24 hr after an i.c.v. injection of 75 microg of colchicine or after repeated i.p. hypertonic saline injections every 8 hr. 4. These studies demonstrate that while alpha1-adrenergic receptors contribute to longterm increases of CRH mRNA levels in the PVN during prolonged stress, other factors are likely to be involved in the stimulation of CRH mRNA following acute stimulation.
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PMID:Role of alpha-1-adrenergic receptors in the regulation of corticotropin-releasing hormone mRNA in the paraventricular nucleus of the hypothalamus during stress. 1110 Sep 76

The short ACTH test is used in evaluating the hypothalamo-pituitary-adrenal axis (HPA-axis) in preterm neonates after dexamethasone treatment. This test mainly examines primary adrenal suppression but is also used as a method to test secondary adrenal insufficiency because long-term deprivation of ACTH causes atrophy of the adrenal cortex. The CRH test, on the other hand, directly examines the function of the pituitary. We tested 18 infants in the neonatal intensive care unit with both the ACTH test and the CRH test to determine which of these two tests more reliably demonstrates HPA-axis suppression. One patient had normal responses both in the ACTH test and in the CRH test when the limit of 360 nmol/L was used as a sign of proper cortisol secretion. In four cases the patients' cortisol secretion would have been regarded as normal by the low-dose ACTH test, whereas the CRH test did not show an adequate cortisol response. In conclusion, the ACTH test did not reliably indicate HPA-axis suppression after a short (<2 weeks) course of dexamethasone therapy in this study. Therefore, whether the infant is or will be under acute stress after short glucocorticoid treatment, ensuring adequate cortisol secretion with the CRH test should be considered.
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PMID:Adrenocorticotropin and corticotropin-releasing hormone tests in preterm infants. 1115 93

Disruption of the blood-brain-barrier (BBB) is important in the pathophysiology of various inflammatory conditions of the central nervous system (CNS), such as multiple sclerosis (MS), in which breakdown of the BBB precedes any clinical or pathological findings. There is some evidence that relapsing-remitting MS attacks may be correlated with certain types of acute stressful episodes. Stress typically activates the hypothalamic-pituitary-adrenal (HPA) axis through the release of corticotropin releasing hormone (CRH), leading to production of glucocorticoids that down regulate immune responses. However, acute stress also has pro-inflammatory effects that appear to be mediated through activation of mast cells. Here we show that acute stress by immobilization increased permeability of rat BBB to intravenous 99Technetium gluceptate (99Tc). This effect was statistically significant in the diencephalon and the cerebellum, while it was absent in the cerebral cortex where there are not mast cells. Immobilization stress also induced activation of mast cells in diencephalon, the site where most mast cells are found in the rat brain. Both BBB permeability and mast cell activation were inhibited by the 'mast cell stabilizer' disodium cromoglycate (cromolyn). These results expand the pathophysiology of mast cells and implicate them in CNS disorders, that may possibly be induced or exacerbated by stress.
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PMID:Acute stress increases permeability of the blood-brain-barrier through activation of brain mast cells. 1114 58

The combined dexamethasone/CRH test (DEX/CRH test) is reported to produce augmented ACTH and cortisol responses in various psychiatric disorders as well as in some non-psychiatric conditions. To examine whether stress affects the outcome of DEX/CRH test, two stress groups in a repeated measures design were compared to an age-matched control group with regard to the psychological, autonomic and neuroendocrine responses after the combined dexamethasone and CRH challenge. Cold pressor (4 degrees C, total 10 min) produced stronger subjective distress than mental arithmetic (15 min). Cold exposure, but not the mental test, elevated systolic and diastolic blood pressure, whereas the mental test increased pulse rate and skin conductance level more markedly than cold exposure. Neither stressor produced a significantly enhanced response of ACTH and cortisol in DEX/CRH test, and there was no correlation between psychological and neuroendocrine responses. These findings suggest that different stressors induce different patterns of sympathetic activation and that acute stress is unlikely to affect the results of DEX/CRH test.
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PMID:Psychological, autonomic and neuroendocrine responses to acute stressors in the combined dexamethasone/CRH test: a study in healthy subjects. 1137 38


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