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

Glycogen is an essential substrate during myocardial anoxia. Since porpranolol may maintain myocardial glycogen levels after acute stress by blockade of catecholamine-induced glycogenolysis, we evaluated the effect of propranolol treatment in the isolated perfused isovolumic paced rat heart. Forty-one rats were studied after 10 min of ice-water immersion: half were pretreated with propranolol, 20 mg/kg/day x3, and half with saline. Glycogen content of unperfused propranolol-treated hearts exceeded controls by 46% (146 +/- 9 vs. 100 +/- 4 mumoles/g dry wt, p less than 0.02), and this difference persisted during aerobic perfusion. Propranolol did not affect adenine nucleotide concentration or left ventricular hemodynamics. Following 5 min of anoxic perfusion, propranolol hearts showed improved ventricular performance concomitant with enhanced glycogenolytic flux and lactate production. Propranolol augmented high energy phosphate production (ATP/AMP = 5.19 +/- 0.42 vs. 3.39 +/- 0.42, p less than 0.02) and increased coronary flow (22.1 +/- 1.6 vs. 16.6 +/- 1.4 ml/min, p less than 0.02) during anoxia. Thus, propranolol supported glycogen stores following acute stresses, enhanced glycogenolytic energy production, increased coronary flow, and improved ventricular function during subsequent anoxia.
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PMID:Protective role of increased myocardial glycogen stores induced by propranolol. 121 34

The present experiment was conducted to determine whether the plasma hormonal and pituitary cyclic AMP responses observed following a single exposure to an acute stressor would diminish following reexposures to the same stressor. Fifteen-min stress exposures (forced running) were separated by 45-min recovery periods. Separate groups of control and stressed animals were sacrificed before and after each of four 15-min stress periods and after each recovery period. The first exposure to 15 min of forced running raised plasma ACTH, corticosterone and pituitary cyclic AMP levels approximately 6-fold and more than tripled levels of plasma prolactin. Plasma ACTH and pituitary cyclic AMP responses to the second, third and fourth stress exposures were very similar to the responses to the first stress exposure, and levels of these substances returned to prestress levels during each 45-min recovery period. Plasma prolactin responses to the four stress sessions were somewhat variable but no significant trend among the responses was seen. Plasma prolactin levels also returned to prestress levels between stress exposures. Corticosterone levels were similar following each of the four stress sessions but levels remained elevated compared to prestress levels between stress exposures. These data suggest that pituitary responses to acute stress are rapid, that return to prestress levels is also rapid, with the exception of corticosterone, and that repeated responses of the same magnitude may be evoked when stressors are separated by short recovery periods.
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PMID:ACTH, prolactin, corticosterone and pituitary cyclic AMP responses to repeated stress. 254 97

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

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

The effects of atropine sulfate pretreatment on pituitary indices of stress response were examined. Pituitary cyclic AMP and plasma prolactin increases following 15 min of acute stress were used as measures of stress response. Over a range of doses (0, 5, 10, 30 and 60 mg/kg), pretreatment with atropine sulfate increased the measured stress responses to footshock but had little or no effect on resting or non-stressed levels of the substances measured. The effects of atropine on response to immobilization were tested only at 5 mg/kg. At this dose, atropine sulfate, but not methylatropine nitrate, increased pituitary cyclic AMP response to immobilization stress demonstrating that the potentiation of the pituitary cyclic AMP stress response was not limited to footshock stress and suggesting that this effect of atropine was central rather than peripheral. Neither atropine nor methylatropine pretreatment at this dose potentiated prolactin response to immobilization stress.
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PMID:Atropine sulfate increases pituitary responses to stress. 303 4

The effects of a 7-day period of daily physical stress (chasing until exhaustion) on the beta-adrenergic response of the rainbow trout (Oncorhynchus mykiss) red blood cell (rbc) were examined in vitro. Physical stress was associated with pronounced increases in the circulating levels of the catecholamine hormones (adrenaline and noradrenaline) measured on days 1, 3 and 7 of the stress regime. After 7 days, the numbers of high-affinity cell surface beta-adrenoceptors were reduced in the physically stressed fish when measured in vitro under conditions of normoxia (20 % reduction) or hypoxia (30 % reduction). Under hypoxic conditions, the binding affinity of the rbc beta-adrenoceptor was significantly higher in the stressed fish. Although the stressed fish had fewer beta-adrenoceptors, rbc adrenergic responsiveness was enhanced after 7 days of physical stress as determined from dose-response curves relating noradrenaline concentration to water and Na+ accumulation (indices of rbc adrenergic Na+/H+ exchange activity). The EC50 values (concentrations yielding half-maximal responses) for noradrenaline were lowered significantly by 1.7- to 3.9-fold in the blood from physically stressed fish. The enhanced adrenergic responsiveness of the rbcs appeared to be unrelated to changes in the initial steps of the beta-adrenergic signal transduction pathway leading to cyclic AMP production because physical stress was without effect on the magnitude or the dose-dependency of rbc cyclic AMP accumulation. To determine whether post-cyclic-AMP events were affected by physical stress, water and Na+ accumulation were measured in rbcs that had been incubated with the permeable cyclic AMP analogue 8-bromo cyclic AMP. The EC50 values for 8-bromo cyclic AMP were lowered by 1.6- to 1.7-fold in the blood from stressed fish. These experiments demonstrate that repeated physical stress significantly enhances the adrenergic responsiveness of the rainbow trout rbc, presumably by modifying the sensitivity of the Na+/H+ exchanger (or the steps immediately preceding exchanger activation) to cyclic AMP. The results are discussed with respect to the interrelationships between chronic and acute stress responses in fish.
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PMID:The effects of repeated physical stress on the b-adrenergic response of the rainbow trout red blood cell 931 46

Stress activates the hypothalamic-pituitary-adrenal (HPA) axis through release of corticotropin releasing factor (CRF), leading to production of glucocorticoids that down regulate immune responses. However, acute stress via CRF also has pro-inflammatory effects. We previously showed that acute stress increases rat blood-brain barrier (BBB) permeability, an effect involving brain mast cells and CRF, as it was absent in W/W(v) mast cell-deficient mice and was blocked by the CRF-receptor antagonist, Antalarmin. We investigated if CRF could also have a direct action on brain microvessel endothelial cells (BMEC) isolated from rat and bovine brain. BMEC were cultured and identified by electron microscopy. Western blot analysis of cultured BMEC identified CRF receptor protein; stimulation with CRF, or it structural analogue urocortin (Ucn) showed that the receptor is functionally coupled to adenylate cyclase as it increased cyclic AMP (cAMP) levels by 2-fold. These findings suggest that CRF could affect BMEC structure or function, as reported for increased cAMP levels by other studies. It is, therefore, possible that CRF may directly regulate BBB permeability, in addition to any effect mediated via brain mast cells.
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PMID:Corticotropin-releasing factor (CRF) can directly affect brain microvessel endothelial cells. 1266 88

Alterations of enzyme activities involved in adenine nucleotide hydrolysis have been reported in spinal cord and blood serum after repeated restraint stress. On the other hand, no effect was observed in the spinal cord of rats after acute stress. In the present study, we investigated the effect of acute stress on the hydrolysis of adenine nucleotides in rat blood serum. Adult male Wistar rats were submitted to 1-h restraint stress and were sacrificed at 0, 6, 24 and 48 h. Increased ATP and ADP hydrolysis were observed in the blood serum of stressed rats 24 h after stress (58% and 54%, respectively, when compared to controls). On the other hand, the AMP hydrolysis was increased after 6 h (68% when compared to controls) and at 24 h (94% when compared to controls) after stress. The results suggest that altered activity of soluble enzymes in serum may be a biochemical marker for stress situations.
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PMID:The effect of stress upon hydrolysis adenine nucleotides in blood serum of rats. 1287 39

Hyperactivity of the stress response has long been recognized as maladaptive. The hippocampus, a brain structure important in mediating this response, is known to be affected by chronic stress, a situation reported to induce changes in adenine nucleotide hydrolysis in the rat. The enzymes catalyzing the hydrolysis of ATP to adenosine in the synaptic cleft are thought to have a role in modulating and controlling synaptic transmission. This study aimed to investigate the effect of acute and repeated restraint stress on the ATP, ADP and AMP hydrolyses in rat hippocampal synaptosomes. Adult male Wistar rats were submitted to acute or repeated (15 and 40 days) stress, and ATPase-ADPase, and 5'nucleotidase activities were assayed in the hippocampal synaptosomal fraction. Acute stress induced increased hydrolyses of ATP (21%), ADP (21%) and AMP (40%). In contrast, ATP hydrolysis was increased by 20% in repeatedly stressed rats, without changes in the ADP or AMP hydrolysis. The same results were observed after 15 or 40 days of stress. Therefore, acute stress increases ATP diphosphohydrolase activity which, in association with 5'-nucleotidase, contributes to the elimination of ATP and provides extracellular adenosine. Interestingly, increased ecto-ATPase activity in response to chronic stress reveals an adaptation to this treatment.
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PMID:Acute and chronic stress alter ecto-nucleotidase activities in synaptosomes from the rat hippocampus. 1521 76

The aim of the present study was to examine the effect of acute restraint stress on rat brain synaptosomal plasma membrane (SPM) ecto-nucleotidase activities at specific stages of postnatal development (15-, 30-, 60- and 90-day-old rats) by measuring the rates of ATP, ADP and AMP hydrolysis 1, 24 and 72 h post-stress. At 1 h after stress NTPDase and ecto-5'-nucleotidase activities were decreased in rats aged up to 60 days old. In adult rats elevated enzyme activities were detected, which indicated the existence of different short-term stress responses during development. A similar pattern of ATP and ADP hydrolysis changes as well as the ATP/ADP ratio in all developmental stages indicated that NTPDase3 was acutely affected after stress. The long-term effect of acute stress on NTPDase activity differed during postnatal development. In juvenile animals (15 days old) NTPDase activity was not altered. However, in later developmental stages (30 and 60 days old rats) NTPDase activity decreased and persisted for 72 h post-stress. In adult rats only ATP hydrolysis was decreased after 24 h, indicating that ecto-ATPase was affected by stress. Ecto-5'-nucleotidase hydrolysing activity was decreased within 24 h in adult rats, while in 15- and 30-day old rats it decreased 72 h post-stress. At equivalent times in pubertal rats (60 days old) a slight activation of ecto-5'-nucleotidase was detected. Our results highlight the developmental-dependence of brain ecto-nucleotidase susceptibility to acute stress and the likely existence of different mechanisms involved in time-dependent ecto-nucleotidase activity modulation following stress exposure. Clearly there are differences in the response of the purinergic system to acute restraint stress between young and adult rats.
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PMID:Effect of acute stress on NTPDase and 5'-nucleotidase activities in brain synaptosomes in different stages of development. 1993 63


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