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

We have used streptozotocin (STZ)-induced diabetes in rats to determine whether this represents a sustained stimulus to the adrenocortical system and whether STZ-diabetic rats are able to mount an acute stress response. Furthermore, we compared pituitary responsiveness to CRF and/or arginine vasopressin, and adrenal responsiveness to ACTH in STZ- vs. vehicle-treated rats. We also compared the efficacy of dexamethasone inhibitory feedback in STZ-diabetic and control rats. Our results show that STZ-treated rats chronically hypersecrete corticosterone (B) as evidenced by their decreased thymus weights, their increased urinary B excretion, and their elevated mean plasma B levels during the light hours of the day. Despite the evidence for sustained hypersecretion of B, STZ-treated rats showed greater and more prolonged ACTH and B responses to the acute stress of histamine injection. However, when tested separately, neither pituitary nor adrenal responsiveness to their secretagogues were increased in STZ-diabetic compared to control rats. Dexamethasone inhibition of stress-induced B secretion was tested using two different paradigms: pentobarbital-anesthetized rats were given iv injections of acid saline, and awake rats were given ip injections of histamine. In both experiments the STZ-treated rats were relatively resistant to glucocorticoid inhibition of stress responses. This finding, taken together with the exaggerated ACTH and B responses to stress, strongly suggests that the facilitatory effects of chronic STZ-diabetes are a consequence of changes in sensitivity of central neural components of the adrenocortical system to stimulatory and/or inhibitory inputs, in conjunction with changes in glucocorticoid feedback sensitivity.
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PMID:Chronic streptozotocin diabetes in rats facilitates the acute stress response without altering pituitary or adrenal responsiveness to secretagogues. 164 14

We have previously shown that exogenous (1 to 5 nmol i.c.v.) PAF induces a rapid increase in plasma ACTH and beta endorphin followed by an increase in plasma corticosterone in conscious rats. The stimulatory action of PAF on the secretion of hypothalamic-pituitary-adrenal (HPA) axis products is mediated at least partly by stimulating hypothalamic CRF release. In addition rat hypothalamic membranes have two populations of specific PAF binding sites. In order to clarify the mode of PAF action on the stress-related hormones, we have now investigated the effect of two PAF antagonists, BN 50739 and RP 52770, on basal and PAF-induced ACTH and corticosterone secretion by conscious rats and on PAF specific binding to rat hypothalamic membranes. The role of PAF as a mediator of neuroendocrine secretion in response to acute stress was examined by determining the effect of PAF antagonists on ether-stress inducing HPA activity. We have also investigated their effect on IL 1-induced HPA activity. The ability of BN 50739 and RP 52770 to displace 3H PAF from its hypothalamic binding sites was correlated with their ability to alter basal hormone secretion and to counteract the PAF-stimulated secretion of HPA axis hormones in vivo (P less than 0.05 by ANOVA). Pretreatment with BN 50739. (50 nmol i.c.v.) did not alter ACTH response to a 1 min ether exposure or to IL1 beta injection (2 nmol i.c.v.). In contrast, RP 52770 (55 nmol i.c.v.) significantly inhibited the ether stress-induced ACTH and corticosterone production by 50% (P less than 0.05). In parallel, pretreatment with RP 52770 (55 nmol i.c.v.) caused a significant inhibition of IL1 beta-induced ACTH secretion. These results suggest that PAF acts, in vivo, on ACTH and corticosterone secretion, through a centrally mediated CRF dependent mechanism involving PAF receptor sites. Additionally, the data also indicate that PAF could have a central role in mediating basal and stress-induced ACTH secretion and that IL 1-induced HPA secretion may be mediated at least in part through the production of PAF.
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PMID:Basal and PAF-, interleukin 1-, ether stress-induced hypothalamic pituitary adrenal secretion of conscious rat: modulation by PAF antagonists. 165 52

Dexamethasone, a synthetic glucocorticoid, has been shown to decrease basal and stress-elevated levels of the pituitary hormone ACTH. Glucocorticoids are known to bind to multiple sites within the brain and pituitary and it is not known which site(s) is most important in mediating the observed inhibition of ACTH release. At the level of the corticotroph, there is contradictory data from in vitro studies regarding whether dexamethasone acts proximal or distal to the formation of the cyclic AMP second messenger that has been shown to be involved in CRF-stimulated ACTH release. In the present report, we have examined the effects of dexamethasone pretreatment on stress-induced elevations in pituitary cyclic AMP and the release of ACTH in vivo. Acute stress (15 min of intermittent footshock) elevated levels of pituitary cyclic AMP and plasma ACTH consistent with previous studies. Dexamethasone administration (0.4 mg/kg 24 hr prior to sacrifice plus 0.2 mg/kg 2 hr prior to sacrifice) inhibited stress-induced elevations in plasma ACTH but did not affect pituitary cyclic AMP response to acute stress. These findings suggest that dexamethasone inhibits the release of ACTH via an action distal to the generation of cyclic AMP.
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PMID:Dexamethasone suppresses ACTH release without attenuating pituitary cyclic AMP response to stress in vivo. 254 93

To study the effect of acute stress on ACTH secretion and synthesis in rat pituitary and hypothalamus, ACTH content and POMC mRNA levels (measured by use of Northern blot analysis) in these tissues as well as the levels of ACTH in plasma and those of CRF in the hypothalamus were determined after insulin-induced hypoglycemia. Plasma ACTH levels increased at 30 and 60 min. ACTH levels in the anterior pituitary lobe (AP) decreased at 30 min, and then returned to control levels at 60 min. No change was seen in the intermediate-posterior pituitary (IP) or the hypothalamus after insulin injection. CRF levels decreased at 30 and 60 min, then returned to control levels at 90 min in the medial basal hypothalamus, including the median eminence. Hybridization with a cDNA probe revealed a single size class of POMC mRNA in AP, IP, and hypothalamus, and the size of POMC mRNA in these tissues did not change during the experimental period. POMC mRNA levels in AP increased at 60 min and reached a peak at 120 min, but those in IP and hypothalamus did not change. These results suggest that 1) insulin-induced hypoglycemia stimulates both secretion and synthesis of ACTH (at least by increasing POMC mRNA levels) in the AP, and 2) the levels of ACTH and POMC mRNA in the IP and hypothalamus are not affected by insulin-induced hypoglycemia.
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PMID:Insulin-induced hypoglycemia increases proopiomelanocortin messenger ribonucleic acid levels in rat anterior pituitary gland. 283 Oct 25

To study the effect of acute stress on CRF release and synthesis in rat hypothalamus, ACTH levels in plasma, CRF contents in the median eminence (ME), and CRF mRNA levels in the hypothalamus without ME and cerebral cortex were determined after insulin-induced hypoglycemia. Plasma ACTH levels increased at 30 and 60 min, while ME CRF content decreased at 30 and 60 min, then returned to the control level at 90 min. Hybridization with a cRNA probe revealed a single size class of CRF mRNA in the hypothalamus and cerebral cortex (approximately 1300 nucleotides), and the size of CRF mRNA in these tissues did not change during the experimental period. CRF mRNA levels in the hypothalamus increased to 130% of the control value at 30 min and reached a peak (186% of the control value) at 120 min, but these levels in the cerebral cortex did not change. These results suggest that insulin-induced hypoglycemia stimulates CRF synthesis by increasing CRF mRNA levels in the hypothalamus as well as CRF release, and that release and synthesis of CRF in the cerebral cortex are independent of those in the hypothalamus.
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PMID:Insulin-induced hypoglycemia increases corticotropin-releasing factor messenger ribonucleic acid levels in rat hypothalamus. 284 Oct 92

Ether-laparotomy stress produced a rapid increase in rat hypothalamic CRF concentration, followed by a rapid reduction and subsequent increase. Cold-restraint stress significantly reduced hypothalamic CRF concentration at 15 min after stress onset. Serum ACTH and corticosterone levels were significantly elevated at 15 min after the onset of both stresses. The CRF responses in the medulla oblongata were not similar to the hypothalamic CRF responses. Norepinephrine concentration in the hypothalamus was reduced, whereas dopamine concentration in the hypothalamus and medulla oblongata was significantly increased. Epinephrine concentrations in these tissues did not show any significant change throughout the stress period. The observations lead to the following conclusions: hypothalamic CRF plays a major role in stimulating ACTH secretion under acute stress; the reduction in hypothalamic CRF is due to an excess release in the early phase of acute stress; hypothalamic CRF and medulla oblongata CRF are controlled by different mechanisms; norepinephrine in the hypothalamus may not be involved in stimulating hypothalamic CRF secretion in the early phase of acute stress; and catecholamines are regulated differently in the hypothalamus and medulla oblongata.
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PMID:Brain corticotropin-releasing factor (CRF) and catecholamine responses in acutely stressed rats. 300 28

We have previously reported that acute stress increases levels of rat pituitary cyclic AMP in vivo. The present study was conducted to test the hypothesis that stress-induced increases in pituitary cyclic AMP in vivo were mediated via CRF. We compared the effects of various stressors with the effects of CRF or epinephrine administration on pituitary cyclic AMP and plasma ACTH responses in vivo. Stressors, epinephrine or CRF increased levels of pituitary cyclic AMP. Pituitary cyclic AMP response to either immobilization or CRF was much greater at light onset than at lights off in rats maintained on a 12 hr light:12 hr dark lighting regimen. In rats with pituitary stalk transections, footshock did not increase levels of pituitary cyclic AMP, suggesting that some factor of central origin was required for this stress response. Exogenous CRF administration did increase levels of pituitary cyclic AMP in stalk-transected rats, while epinephrine increased levels in sham-operated but not in stalk-transected rats. Antisera to CRF markedly decreased pituitary cyclic AMP response to exogenous CRF administered 6 min following antisera and partially attenuated pituitary cyclic AMP response to forced running. Taken as a whole these data support a major role for CRF in the pituitary cyclic AMP response to stress.
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PMID:Comparison of the effects of CRF and stress on levels of pituitary cyclic AMP and plasma ACTH in vivo. 303 31

A variety of chronic stress paradigms have been shown to increase basal activity in the hypothalamic-pituitary-adrenocortical axis, resulting in hypercorticoidism. Despite this, chronically stressed rats typically exhibit facilitated ACTH responses to acute novel stress, suggesting that the activity of some central neural component(s) in the axis is facilitated by chronic stress. We have used the chronic stress of streptozotocin (STZ)-induced diabetes in rats to determine diurnal sensitivity of basal and stimulated ACTH secretion to exogenous corticosterone (B) feedback in vivo. Control and STZ-diabetic rats were adrenalectomized or adrenalectomized and implanted with a 30% or 50% B pellet at the time of vehicle/STZ injection. Rats were killed 5 days later, under basal conditions or after 6 min of restraint, in the morning or evening. We show that basal ACTH secretion in both the morning and evening was similarly suppressed by B in STZ-diabetic and control rats. However, stress-induced ACTH secretion was significantly greater in STZ-diabetic compared to control rats throughout the range 3-7 micrograms/dl B, when tested in the morning. Suppression of evening stress-induced ACTH secretion by B was also significantly different in STZ-diabetic rats; however, the IC50 values for the inhibition of ACTH by B did not differ. This result shows that in the evening after stress and under basal conditions in both the morning and evening, sensitivity to B feedback is normal in chronically stressed, STZ-diabetic rats. Despite the observed facilitation of morning stress-induced ACTH secretion in STZ-diabetic rats, there were no differences in hypothalamic CRF content between control and STZ-diabetic tissue. We conclude that 1) the facilitatory input to the paraventricular nucleus functions primarily at the time of the circadian trough to maintain or enhance acute stress responsiveness in chronically stressed, hypercorticoid rats; and 2) the sensitivity of ACTH to inhibition by B is normal in rats chronically stressed by STZ-induced diabetes.
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PMID:Streptozotocin-diabetic rats exhibit facilitated adrenocorticotropin responses to acute stress, but normal sensitivity to feedback by corticosteroids. 824 90

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

The effects of acute stress on various indices of sympatho-adrenal, sympathoneural functions and hypothalamic-pituitary-adrenal (HPA) axis were examined both at central and peripheral sites in healthy, intact male Fischer 344/N rats of increasing age. Extracellular fluid (ECF) levels of norepinephrine (NE), its metabolites dihydroxyphenylglycol (DHPG), and methoxyhydroxyphenylglycol (MHPG), and of the dopamine metabolite dihydroxyphenylacetic acid (DOPAC), were measured 24 h after implantation of a microdialysis probe in the paraventricular nucleus (PVN) of the hypothalamus, and samples collected at 30-min. intervals during immobilization (IMMO). ECF levels of NE, DHPG, MHPG, and DOPAC were at baseline similar in both age groups, and all increased significantly in response to IMMO. The IMMO-induced increases in ECF levels of NE and MHPG were, however, significantly smaller in old than in young rats. Plasma levels of the dihydroxyphenylalanine (DOPA), -NE, epinephrine (EPI), DHPG, MHPG, dopamine (DA), DOPAC and HVA, were determined in different groups of young and old rats, cannulated in the tail artery, at baseline, and after 5, 30, 60, and 120 min of IMMO. Basal levels of DOPA, DHPG, MHPG, DA, DOPAC, HVA, NE and EPI were significantly higher in old than in young rats, and increased in plasma during IMMO. However, the magnitude of the increase in the majority of these compounds was significantly smaller in old than in young rats. Basal plasma levels of ACTH were similar among age groups, and basal plasma levels of corticosterone showed a significant aging-associated decline. Two i.v. doses (2 and 20 micrograms/kg BW) of rat CRF elicited significantly greater and delayed ACTH, and greater corticosterone responses in older rats, consistent with the pattern encountered in hypothalamic CRF deficiency. An i.v. injection of ACTH evoked lower corticosterone responses in the older (18 and 24 month old) than in the younger (2 and 8 month old) groups of rats, consistent with secondary adrenocortical atrophy in older animals. Steady-state mRNA levels of mineralocorticoid and glucocorticoid receptors were significantly decreased in the hippocampus of the 8-, 18-, and 24-month-old rats, compatible with maturational rather than senescent changes. CRF mRNA levels in the paraventricular nucleus of the hypothalamus, and levels of POMC mRNA in the anterior pituitary were significantly reduced with age. In conclusion, in this strain of rats, aging is associated with diminished responsiveness of central, and peripheral catecholaminergic systems to acute stress, and progressive hypothalamic CRH deficiency.
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PMID:Aging is associated in the 344/N Fischer rat with decreased stress responsivity of central and peripheral catecholaminergic systems and impairment of the hypothalamic-pituitary-adrenal axis. 859 25


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