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PubMed2000

pH, abscisic acid and the integration of metabolism in plants under stressed and non-stressed conditions: cellular responses to stress and their implication for plant water relations.

A paradigm for the response of plants to stress is presented which suggests that plants move towards a state of minimal metabolic activity as a stress intensifies and remain in that state until that stress is relieved. The paradigm is based on the proposition that cells that interface with the transpiration stream employ variations on the following theme to move towards that state. Tension on the apoplastic water opens a mechanosensitive Ca2+ channel, a response that is augmented by apoplastic ABA. The resulting elevated cytoplasmic Ca2+ deactivates a plasmalemma H+/ATPase and also activates a K(+)-H+ symport. The inflow of K+ and H+ depolarizes the membrane and renders the apoplast less acidic, the protons being removed to the vacuole and the K+ ions being re-exported via the K+ outward rectifying channel. The onset of darkness in guard and mesophyll cells deactivates the plasmalemma H+/ATPase and then the events outlined above ensue except that these cells do not appear to utilize either Ca2+ or ABA during these changes. In stressed cells it is proposed that elevated cytoplasmic Ca2+ activates the release of an ABA precursor from a stored form. ABA is then released in the apoplast after export of the precursor if the activity of the K(+)-H+ symport has brought the apoplastic pH close to 7.0. It is proposed that aquaporins in the xylem parenchyma and mesophyll cells are opened by elevated cytoplasmic Ca2+ when the water potential of the transpiration stream is high so that water can be stored in the 'xylem parenchyma reservoir'. The water in this reservoir is then used to increase the water potential in the transpiration stream when the water column is under tension and to help repair embolisms by a mechanism that resembles stomatal closure.

Abscisic Acid↗
PubMed1984

Stress, cortisol, interferon and "stress" diseases. I. Cortisol as the cause of "stress" diseases.

An attempt is made to define a biochemical formula for stress, as an overproduction of cortisol +/- impaired interferon response. The behavior Type A individual under stress, would exhibit elevated levels of cortisol with normal interferon response, whereas the Type C individual, would exhibit elevated levels of cortisol and impaired interferon responses. Evidence is presented that elevated levels of cortisol manufactured chronically under the affect of stress, and regardless of the type of individual affected, are a cause or the cause of chronic diseases, and not the result of same. This evidence would show that: Elevated levels of cortisol precede certain diseases, and do not follow them, when cortisol is checked out for this purpose in pre-disease conditions. When elevations of cortisol levels are induced through long-term corticosteroids therapy, in patients suffering of diseases requiring this type of treatment, conditions mimicking chronic diseases, would appear. When corticosteroids therapy would be discontinued, the "chronic diseases" mentioned above would disappear. When pharmaceuticals with potential cortisol antagonistic capabilities, were used in diseases totally unrelated, but having in common, elevated levels of cortisol, alleviation of symptoms and/or diseases would occur.

Cushing Syndrome↗
PubMed2006

Impact of an intense stress on ethanol consumption in female rats characterized by their pre-stress preference: modulation by prenatal stress.

We examined the influence of prenatal stress on alcohol preference in adult female rats exposed to an intense stress. To take into account interindividual variability, the study was conducted in animals categorized as low or high alcohol preferring. After footshock, control high-preferring rats strongly reduced their alcohol consumption; in contrast, alcohol consumption was not changed in high-preferring rats that were prenatally stressed.

Adaptation, Psychological↗
PubMed2006

Stressing the obvious? Cell stress and cell stress proteins in cardiovascular disease.

It is only some forty years since the discovery of the heat shock or cell stress response and just over twenty years since the heat shock/cell stress response was linked to protein misfolding. The plethora of intracellular proteins which promote correct protein folding in the cell, variously termed molecular chaperones, heat shock proteins, or cell stress proteins, have only been identified in the last fifteen years. During this period it has also been discovered that: (i) molecular chaperones are potent immunogens with immunomodulatory activity and (ii) they can be secreted by cells and exhibit intercellular signaling actions. These various functions of molecular chaperones are increasingly being linked to the pathology of the cardiovascular system. Molecular chaperones within cells can exhibit cardioprotection if their levels are artificially elevated, suggesting that these proteins may have therapeutic activity. In contrast, there is evidence that atherogenesis may be linked to immunity to one specific molecular chaperone, Hsp60. This may offer the possibility of treating atherosclerosis by vaccination. However, there is also growing evidence that secreted molecular chaperones have pro- or anti-inflammatory actions that are relevant to cardiovascular pathology. This review brings these various strands of research together to provide an overview of the role of molecular chaperones in cardiovascular disease.

Animals↗
PubMed1998

Stimulation of "stress-regulated" mitogen-activated protein kinases (stress-activated protein kinases/c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses.

"Stress-regulated" mitogen-activated protein kinases (SR-MAPKs) comprise the stress-activated protein kinases (SAPKs)/c-Jun N-terminal kinases (JNKs) and the p38-MAPKs. In the perfused heart, ischemia/reperfusion activates SR-MAPKs. Although the agent(s) directly responsible is unclear, reactive oxygen species are generated during ischemia/reperfusion. We have assessed the ability of oxidative stress (as exemplified by H2O2) to activate SR-MAPKs in the perfused heart and compared it with the effect of ischemia/reperfusion. H2O2 activated both SAPKs/JNKs and p38-MAPK. Maximal activation by H2O2 in both cases was observed at 0.5 mM. Whereas activation of p38-MAPK by H2O2 was comparable to that of ischemia and ischemia/reperfusion, activation of the SAPKs/JNKs was less than that of ischemia/reperfusion. As with ischemia/reperfusion, there was minimal activation of the ERK MAPK subfamily by H2O2. MAPK-activated protein kinase 2 (MAPKAPK2), a downstream substrate of p38-MAPKs, was activated by H2O2 to a similar extent as with ischemia or ischemia/reperfusion. In all instances, activation of MAPKAPK2 in perfused hearts was inhibited by SB203580, an inhibitor of p38-MAPKs. Perfusion of hearts at high aortic pressure (20 kilopascals) also activated the SR-MAPKs and MAPKAPK2. Free radical trapping agents (dimethyl sulfoxide and N-t-butyl-alpha-phenyl nitrone) inhibited the activation of SR-MAPKs and MAPKAPK2 by ischemia/reperfusion. These data are consistent with a role for reactive oxygen species in the activation of SR-MAPKs during ischemia/reperfusion.

Amino Acid Sequence↗
PubMed2005

[Stress management among hospital nurses--stress & stress-coping scale (SSCQ) as applied to nurses].

The purpose of this study was to evaluate the validity of the Stress and Stress-Coping Questionnaire (SSCQ) for female nursing groups. Subjects were 300 female nurses employed at hospitals. Mean age was 32.9 +/- 8.9 yr and mean number of years of work experience was 11.9 +/- 8.0 yr. Data for the study were collected via the self-completed SSCQ, which all subjects completed. In order to asses the validity of the SSCQ, subjects were also asked to complete a 60-question General Health Questionnaire (GHQ) that assessed mental well being. Based on the results of factor analysis, the original version of the SSCQ, comprising 153 questions in 10 subscales, was revised to the nurse-specific SSCQ-N, comprising 123 questions and 15 subscales. Cronbach's alpha coefficient for subscales varied from 0.70 to 0.83, showing a significant correlation with the point score of the GHQ, for demonstrating criterion-related validity in the SSCQ. These results verify the usefulness for female nursing groups of the SSCQ for assessing mental well being and suggesting ways to manage stress in nurses.

Adaptation, Psychological↗
PubMed1993

Comparison of dobutamine stress echocardiography, dipyridamole stress echocardiography and exercise stress testing for diagnosis of coronary artery disease.

To compare the value of dobutamine and dipyridamole stress echocardiography with exercise stress testing for the diagnosis of coronary artery disease (CAD), 80 patients with chest pain of suspected myocardial ischemic origin (57 with CAD and 23 without significant CAD) underwent dobutamine stress echocardiography (5 to 40 micrograms/kg/min), dipyridamole echocardiography (0.84 mg/kg over 10 minutes) and bicycle exercise electrocardiography after discontinuation of antianginal treatment. Dobutamine echocardiography and exercise testing revealed a higher overall sensitivity than dipyridamole echocardiography (79 vs 60%, p < 0.005; 77 vs 60%, p < 0.05, respectively); this finding was due to a higher dobutamine and exercise sensitivity in 1-vessel CAD (62 vs 33%, p < 0.05 for both tests), whereas sensitivity of the 3 tests was similar in multivessel CAD. Dobutamine and dipyridamole showed a higher specificity than exercise (83 vs 43%, p < 0.01; 96 vs 43%, p < 0.005, respectively). Diagnostic accuracy of dobutamine echocardiography was higher than that of exercise (80 vs 67%, p < 0.05), whereas the difference with dipyridamole (80 vs 70%) was not significant. In the tests that yielded positive results, double product during exercise was significantly higher than that during dobutamine and dipyridamole echocardiography. No major complications occurred during the tests, but adverse effects were more frequent during dobutamine testing. Thus, dobutamine echocardiography may be superior to dipyridamole echocardiography and exercise electrocardiography for the diagnosis of CAD.

Adult↗
PubMed2004

Postnatal stress in mice: does "stressing" the mother have the same effect as "stressing" the pups?

Short- and long-term effects of brief maternal separation, maternal exposure to novel male odor, and standard rearing were compared in NMRI mice. The first condition consisted of 15 min of daily exposure of pups to clean bedding (CB), and the second condition consisted of 15 min of mothers' exposure to the odor of strange males (SM), for 14 days after birth starting from postnatal Day 1. Thus, both conditions entailed the same period of maternal separation. A control mother-offspring group was left undisturbed (nonhandled, N-H). Corticosterone levels of mothers and pups were measured at the end of the last manipulation session. Corticosterone levels were higher in SM mothers, differing from both those of CB and of control dams; CB pups showed the highest corticosterone levels in comparison with the pups belonging to the other groups. Maternal behavior observed as furthest as possible from the daily separation session did not differ among the three groups. The behavioral response to 0.5 mg/kg of apomorphine in 15-day-old pups was enhanced in both CB and SM animals, which suggests an alteration of dopaminergic functioning. Finally, adult CB and SM male mice showed an increase in the percentage of time and entries into the open arms of the plus-maze in comparison to nonhandled males. This study indicates that exposure to ecologically relevant stimuli elicited a stress response in lactating dams. This "social stress" brings about short- and long-term effects in the offspring, even in the absence of any direct manipulation of the pups.

Animals↗
PubMed2006

Desiccation and zinc binding induce transition of tomato abscisic acid stress ripening 1, a water stress- and salt stress-regulated plant-specific protein, from unfolded to folded state.

Abscisic acid stress ripening 1 (ASR1) is a low molecular weight plant-specific protein encoded by an abiotic stress-regulated gene. Overexpression of ASR1 in transgenic plants increases their salt tolerance. The ASR1 protein possesses a zinc-dependent DNA-binding activity. The DNA-binding site was mapped to the central part of the polypeptide using truncated forms of the protein. Two additional zinc-binding sites were shown to be localized at the amino terminus of the polypeptide. ASR1 protein is presumed to be an intrinsically unstructured protein using a number of prediction algorithms. The degree of order of ASR1 was determined experimentally using nontagged recombinant protein expressed in Escherichia coli and purified to homogeneity. Purified ASR1 was shown to be unfolded using dynamic light scattering, gel filtration, microcalorimetry, circular dichroism, and Fourier transform infrared spectrometry. The protein was shown to be monomeric by analytical ultracentrifugation. Addition of zinc ions resulted in a global change in ASR1 structure from monomer to homodimer. Upon binding of zinc ions, the protein becomes ordered as shown by Fourier transform infrared spectrometry and microcalorimetry, concomitant with dimerization. Tomato (Solanum lycopersicum) leaf soluble ASR1 is unstructured in the absence of added zinc and gains structure upon binding of the metal ion. The effect of zinc binding on ASR1 folding and dimerization is discussed.

Amino Acid Sequence↗
PubMed1982

Stress-induced inhibition of the plasma corticosterone response to a subsequent stress in rats: a nonadrenocorticotropin-mediated mechanism.

The present study was designed to define further the relationships between ACTH and corticosterone secretion after repeated administration of a discrete restraint stress in rats. The possibility that plasma ACTH and corticosterone responses to stress may be modified by prior exposure to stress was examined in male rats using a 2-min restraint stress. The peak plasma ACTH response to a single restraint stress occurred at 2.5-5 min after the onset of the stress, and plasma ACTH returned to the basal concentration by 30 min. The plasma corticosterone concentration after this stress peaked at 15-30 min and returned to the control range by 60-90 min. The time courses of the plasma ACTH and corticosterone responses to restraint stress after administration of three prior stresses at 90-min intervals were similar to those after a single stress. Stress-induced increments in plasma concentrations of ACTH and corticosterone were similar in rats that received either a single restraint stress or as many as seven stresses repeated at 90-min intervals. Next, we examined the plasma ACTH and corticosterone responses to repeated stress applied at intervals of less than 90 min (30 or 60 min), that is, at times at which the plasma corticosterone concentration had not yet returned to basal levels. The plasma ACTH responses to the second stress were similar in magnitude and duration to the response after a single stress, whether the second stress was applied 30, 60, or 90 min after the first stress. The plasma corticosterone response to a second stress applied at 90 min was identical to the response after the initial stress. In contrast, the plasma corticosterone responses to a second stress applied 30 or 60 min after the initial stress were markedly reduced. The decrease in plasma corticosterone response to the second stress did not result from a decrease in secretion of bioactive ACTH; no difference was found between the magnitude of the plasma ACTH response to the initial stress and a subsequent stress applied 30 min later using either bioassay or immunoassay measurements. Also, the rate of corticosterone catabolism was not increased by prior stress; the rate of disappearance of corticosterone from plasma was identical after an initial or a subsequent stress applied at 30 min. We were unable to demonstrate decreased adrenocortical responsiveness to ACTH after an initial stress in dexamethasone-suppressed rats; in these rats the plasma corticosterone response to exogenous ACTH was not decreased by prior restraint stress. These data clearly define a period of decreased adrenocortical response to subsequent stress after stress-induced activation of adrenocortical secretion. Furthermore, this altered adrenocortical response appears to be mediated by a nonadrenocorticotropin mechanism.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[Effect of adaptation to brief stress exposure on the realization of the stress reaction, impairment of metabolism and myocardial contraction caused by prolonged emotional-pain stress].

Adaptation of animals to short-term stressory actions was shown to prevent an excessive stimulation of adrenergic and hypophysis-adrenal system, impairments of oxidation and phosphorylation in heart muscle mitochondria as well as the contractile function of heart muscle, occurred after the prolonged emotional-painful stress.

Adaptation, Physiological↗
PubMed2000

Evolution in stressful environments. I. Phenotypic variability, phenotypic selection, and response to selection in five distinct environmental stresses.

Considerable debate has accompanied efforts to integrate the selective impacts of environmental stresses into models of life-history evolution. This study was designed to determine if different environmental stresses have consistent phenotypic effects on life-history characters and whether selection under different stresses leads to consistent evolutionary responses. We created lineages of a wild mustard (Sinapis arvensis) that were selected for three generations under five stress regimes (high boron, high salt, low light, low water, or low nutrients) or under near-optimal conditions (control). Full-sibling families from the six selection histories were divided among the same six experimental treatments. In that test generation, lifetime plant fecundity and six phenotypic traits were measured for each plant. Throughout this greenhouse study, plants were grown individually and stresses were applied from the early seedling stage through senescence. Although all stresses consistently reduced lifetime fecundity and most size- and growth-related traits, different stresses had contrasting effects on flowering time. On average, stress delayed flowering compared to favorable conditions, although plants experiencing low nutrient stress flowered earliest and those experiencing low light flowered latest. Contrary to expectations of Grime's triangle model of life-history evolution, this ruderal species does not respond phenotypically to poor environments by flowering earlier. Most stresses enhanced the evolutionary potential of the study population. Compared with near-optimal conditions, stresses tended to increase the opportunity for selection as well as phenotypic variance, although both of these quantities were reduced in some stresses. Rather than favoring traits characteristic of stress tolerance, such as slow growth and delayed reproduction, phenotypic selection favored stress-avoidance traits: earlier flowering in all five stress regimes and faster seedling height growth in three stresses. Phenotypic correlations reinforced direct selection on these traits under stress, leading to predicted phenotypic change under stress, but no significant selection in the control environment. As a result of these factors, selection under stress resulted in an evolutionary shift toward earlier flowering. Environmental stresses may drive populations of ruderal plant species like S. arvensis toward a stress-avoidance strategy, rather than toward stress tolerance. Further studies will be needed to determine when selection in stressful environments leads to these alternative life-history strategies.

Biological Evolution↗
PubMed2005

Comparison of prognostic value of stress echocardiography versus stress electrocardiography in patients with suspected coronary artery disease.

Stress electrocardiographic (ECG) ST-segment depression is a prognostic marker of adverse cardiac outcomes in coronary artery disease. However, use of concurrent stress echocardiography (ECHO) has lead to concordant and discordant findings on stress electrocardiogram during stress studies. The prognostic value of stress ECHO in the setting of these stress ECG findings has not been previously evaluated. Outcomes of 1,268 patients (60 +/- 12 years old, 48% women) who had normal electrocardiograms and underwent stress ECHO were analyzed. ST-segment depression > or =1.5 mm in 2 contiguous leads on stress electrocardiogram and a wall motion score index of >1 on peak stress echocardiogram were considered abnormal. Events of nonfatal myocardial infarction (n = 18) and cardiac death (n = 32) were analyzed during follow-up (2.8 +/- 0.9 years). In 91 patients (7%) who had abnormal findings on stress electrocardiogram, 38 (41%) had an abnormal finding on stress echocardiogram and 4 had cardiac events (0.6% per year), and all who had a normal finding on stress echocardiogram had no events (n = 53, 59%, p = 0.01). Among 46 events (92%) with a normal finding on stress electrocardiogram, 30 (60%) showed a discordantly abnormal finding on stress echocardiogram (3.2% per year, p <0.01). Overall, the cohort that had normal findings on stress echocardiogram showed a lower event rate (72%, 16 events, 1.1% per year) compared with the cohort that had abnormal findings on stress echocardiogram (28%, 34 events, 3.6% per year, p <0.001), independent of stress ECG response. Peak wall motion score index (hazard ratio 2.55, p <0.001) and left ventricular ejection fraction (hazard ratio 0.99, p <0.001) were independent and incremental (global chi-square, p <0.001) prognostic markers by stress ECHO. In conclusion, a normal finding on stress echocardiogram confers a benign prognosis independent of the type of stress ECG response during stress studies. In addition, peak wall motion score index and ejection fraction by ECHO are stronger prognostic markers over stress electrocardiography in patients who are evaluated for coronary artery disease.

Adult↗
PubMed2007

Preconditioning stress prevents cold restraint stress-induced gastric lesions in rats: roles of COX-1, COX-2, and PLA2.

We investigated the protective effect of mild stress on gastric lesions induced by cold-restraint stress, especially concerning prostaglandins (PGs)/cyclo-oxygenase (COX) isozymes. Rats were exposed to severe stress (cold-restraint stress at 10 degrees C for 6 hr) or mild stress (cold-restraint stress at 10 degrees C for 30 min and kept at room temperature for 60 min) followed by severe stress. Severe stress induced gastric lesions, with a concomitant decrease in body temperature (BT). The ulcerogenic response was inhibited by atropine but worsened by indomethacin and SC-560 but not rofecoxib, although none of these agents had any effect on the change in BT. Mild stress suppressed the gastric ulceration and the decrease in BT induced by severe stress, and these effects were reversed by both COX-1 and COX-2 inhibitors. The expression of COX-2 in the stomach was up-regulated from 4 hr after severe stress and this response was slightly expedited by mild stress. COX-2 was also expressed in the hypothalamus under normal and stressed conditions. Quinacrine (phospholipase A(2) inhibitor) attenuated the protective effect of mild stress on the ulceration and decrease in BT caused by severe stress. TA-0910 (TRH analogue) at a low dose also prevented the gastric ulceration and the decrease in BT induced by severe stress. These results suggest that mild stress protects against cold-restraint stress-induced gastric ulceration, and the effect is peripherally and centrally mediated by PGs derived from both COX-1 and COX-2 through the activation of phospholipase A(2). TRH may also be involved in the protective effect of mild stress, probably through regulation of the thermogenic system.

Animals↗
PubMed2005

Permanent alterations in stress responsivity in female offspring subjected to combined maternal lead exposure and/or stress.

Elevated lead (Pb) exposures preferentially impact low socioeconomic status (SES) populations, the same groups thought to sustain the highest levels of environmental stress. As co-occurring risk factors, therefore, Pb and stress could interact, a possibility further supported by the fact that both act on mesocorticolimbic dopamine systems of the brain. We recently demonstrated in rats that maternal Pb exposure could permanently increase basal corticosterone levels of offspring consistent with altered hypothalamic pituitary adrenal (HPA) axis function. The current study was thus designed to test the hypothesis that stress responsivity of offspring should likewise be altered, with the outcome differing in response to Pb, stress or Pb+stress. The impact of intermittent variable stress challenges (restraint, novelty, cold) on behavior sensitive to Pb exposure (fixed interval (FI) schedule-controlled responding) and on stress-induced corticosterone changes were evaluated in adult female offspring of dams that had been exposed to Pb (150 ppm) in drinking water from 2 months prior to breeding through lactation with or without maternal restraint stress on days 16 and 17 of gestation. This design yielded four treatment groups: (NS/0, no maternal Pb, no maternal stress; S/0, no maternal Pb, maternal stress; NS/150, maternal Pb, no maternal stress; and S/150, maternal Pb exposure and maternal stress). While maternal Pb alone and stress alone each altered components of stress responsivity, the greatest number of effects was seen in response to Pb + stress. This included alterations in FI performance following both restraint and cold stress and in the corticosterone response to cold stress. Collectively, these studies reveal that maternal Pb exposure alone can permanently alter stress responsivity and that the profile of effects produced by maternal Pb differ from those produced by maternal Pb in conjunction with stress, findings which have both mechanistic and risk assessment significance.

Animals↗
PubMedDate not supplied

Combined analysis of resting regional wall thickening and stress perfusion with electrocardiographic-gated technetium 99m-labeled sestamibi single-photon emission computed tomography: prediction of stress defect reversibility.

BACKGROUND: The high photon flux and stable distribution of the myocardial perfusion agent 99mTc-labeled sestamibi allow the perfusion data to be acquired in an electrocardiographic (ECG)-gated mode, such that information on resting regional wall thickening may be obtained simultaneously with stress perfusion data. The objective of this study was to assess whether visual analysis of resting regional wall thickening provided by ECG-gated acquisition of 99mTc-labeled sestamibi stress perfusion images correlates with and predicts the reversibility of stress-induced perfusion defects, potentially obviating the need for rest imaging. METHODS AND RESULTS: Fifty-nine patients referred for myocardial perfusion imaging were studied with rest and stress single-photon emission computed tomographic (SPECT) sestamibi imaging, and the stress perfusion data were acquired in an ECG-gated mode. Visual analysis of the presence and reversibility of stress perfusion defects on standard imaging was correlated with the wall thickening data from the poststress gated SPECT images. Quantitative circumferential profile analysis of the short-axis images was performed to assess the influence of relative stress perfusion defect severity on the correlation between wall thickening and defect reversibility. Among the 72 segments with stress-induced perfusion defects and visually apparent wall thickening on ECG-gated SPECT images, 69 were reversible on rest imaging (positive predictive value of 96% for wall thickening to predict stress defect reversibility). Of the 35 segments with stress-induced defects and no apparent wall thickening on ECG-gated SPECT images, however, 14 (40%) demonstrated significant stress defect reversibility on rest imaging. This result represents a negative predictive value of only 60% for the lack of apparent wall thickening to predict correctly an irreversible stress defect. Among the segments with reversible stress perfusion defects and visually apparent wall thickening, relative stress sestamibi activity was higher (51% +/- 10% [percentage of peak]) than in segments with reversible stress defects and no visually apparent wall thickening (39% +/- 4% of peak activity [p < 0.0001]). CONCLUSIONS: Visual evidence of wall thickening by poststress ECG-gated SPECT sestamibi imaging in the territory of a stress-induced perfusion defect correlates highly with stress defect reversibility on rest imaging and may obviate the need to perform rest imaging, thereby potentially reducing the time and cost involved in myocardial perfusion imaging. The absence of visually apparent wall thickening, however, underestimates the prevalence of stress defect reversibility on rest imaging; in such instances, rest imaging must be performed to differentiate ischemia from infarction in the territory of a stress perfusion defect.

Adult↗
PubMed2006

Ang II and Ang III modulate PTZ seizure threshold in non-stressed and stressed mice: possible involvement of noradrenergic mechanism.

The present study evaluated the effects of Angiotensin (Ang) Ang II and Ang III on pentylenetrazol (PTZ) seizure threshold in non-stressed and stressed mice as well as the possible participation of noradrenergic (NA) mechanism in their effects. While intracerebroventricular (i.c.v.) administered Ang II and Ang III increased the PTZ threshold for myoclonic twitch (MTW), generalized clonus (GNCL) and tonic hindlimb extension (THE) in non-stressed mice, they attenuated the anticonvulsant effects of acute restraint stress. The selective AT(1) receptor antagonist losartan rather than the selective AT(2) receptor antagonist PD 123319 antagonized the effects of Ang II in both non-stressed and stressed animals. Losartan also reversed the effects of Ang III on the thresholds for MTW and GNCL in stressed mice. Concurrent administration of desipramine (NA-uptake inhibitor) and either Ang II or Ang III produced a greater effect on MTW and GNCL in non-stressed mice. However, desipramine reversed the peptide-induced attenuation on PTZ seizure threshold in stressed mice. Prazosin (alpha(1)-adrenoreceptor (AR) antagonist) blocked the effects of Ang II on PTZ seizure threshold for the three convulsive phases in both non-stressed and stressed mice. Prazosin potentiated the anti-seizure effect of Ang III against MTW, GNCL, and THE in non-stressed mice while it reversed the seizure threshold-decreasing effect of this heptapeptide on MTW and GNCL in stressed mice. Yohimbine (alpha(2)-AR antagonist) blocked only the effects exerted by Ang II on the PTZ seizure threshold in non-stressed mice. Our findings suggest that the responses of Ang II and Ang III on PTZ seizure threshold can be mediated by AT(1) receptors in non-stressed and even more in stressed mice. We also hypothesize that the NA-dependent mechanism plays a major role in the effects of Ang peptides in both non-stressed and stressed mice.

Adrenergic Uptake Inhibitors↗
PubMed2004

Stress-induced modulation of skin immune function: two types of antigen-presenting cells in the epidermis are differentially regulated by chronic stress.

BACKGROUND: Inflammatory skin diseases are exacerbated by psychiatric stress. Previous studies have shown that the activity of epidermal antigen-presenting cells (APCs), Langerhans cells (LCs) and keratinocytes (KCs), is affected by stress. Hapten application causes migration of LCs to draining lymph nodes (DLNs). Recently, we found that hapten application also activates epidermal cells (ECs) to mature potent APCs, and that the main APCs in these populations are KCs. Thus, DLN cells and ECs following hapten application are available for estimating the APC function of LCs and KCs in stress studies. OBJECTIVES: To investigate the mechanism of exacerbation of skin inflammation by chronic stress by observing the effect of isolation stress transversally on the skin immune and neurohormonal systems. METHODS: Contact sensitivity (CS) was elicited in BALB/c mice. The APC function of LCs and ECs following hapten application was assessed by the CS-inducing activity in the recipient mice. Levels of neurohormonal transmitters and proinflammatory cytokines were measured by enzyme-linked immunosorbent assay. Cell surface molecules were detected using flow cytometry. Expression of mRNA for cytokines, neurohormonal receptors and a differentiation marker by ECs was determined by reverse transcription-polymerase chain reaction. RESULTS: Acute stress (2-day isolation) suppressed induction of CS, while chronic stress (30-day isolation) markedly enhanced induction of CS. DLN cells from chronically stressed mice contained increased numbers of LCs and exhibited enhanced APC function for inducing CS. In contrast, the APC function of KCs from these mice was markedly suppressed. Serum corticosterone levels were enhanced in acute stress, while substance P (SP) levels were enhanced in chronic stress. Corticotrophin-releasing hormone receptor-1 mRNA expression in ECs was enhanced in acute stress, while SP receptor (i.e. neurokinin-1 receptor) mRNA expression in ECs was enhanced in chronic stress. Production and mRNA expression of the proinflammatory cytokines interleukin-1 alpha and tumour necrosis factor-alpha by ECs following hapten application was markedly suppressed in chronic stress. Expression by ECs of E-cadherin, which adheres LCs and KCs homophilically, was suppressed in chronic stress. In addition, these cells exhibited impaired differentiation, i.e. suppressed spontaneous proliferation and enhanced mRNA expression for transglutaminase-3. CONCLUSIONS: Chronic isolation stress may enhance CS responses by upregulation of the APC activity of LCs and the SP system. However, dysregulation of KC function and differentiation by chronic stress suggests that KCs may not contribute to the enhancement of the CS response positively. These complex changes suggest that chronic isolation stress in mice may provide a possible model system for studying the mechanism of exacerbation of skin inflammation by stress.

Animals↗