Sympatho-adrenomedullary System Research Articles

Cognitive performance during exposure to moderate normobaric hypoxia after sleep restriction: relationship to physiological and stress biomarkers

IntroductionExposure to moderate levels of simulated hypoxia has subtle cognitive effects relative to ground level, in healthy individuals. However, there are few data on the cognitive consequences of the combination of hypoxia and partial sleep deprivation, which is a classic military or civilian operational context. In this study, we tested the hypothesis that exposure to moderate hypoxia while sleep-restricted impairs several domains of cognition, and we also assessed physiological parameters and salivary concentrations of cortisol and alpha-amylase. MethodSeventeen healthy males completed two sessions of cognitive tests (sustained attention using the PVT psychomotor vigilance task and executive functions using the Go-NoGo inhibition task and N-Back working memory task) after 30 minutes (T+30’) and 4 hours (T+240’) of exposure in a normobaric hypoxic tent (FIO2 = 13.6%, ≃ 3,500 m) (HY). This was completed after one night of sleep restriction (3 a.m. to 6 a.m. bedtime, SRHY) and one night of habitual sleep (10 p.m. to 6 a.m. bedtime, HSHY) (with cross-over randomization). The two nights sleep architecture and physiological parameters (oxygen saturation (SpO2) and heart rate (HR) during T+30’ and T+240’sessions were analyzed. Salivary cortisol and alpha-amylase (sAA) concentrations were analyzed before hypoxia, after the T+30’ and T+240’ cognitive sessions, and after leaving the hypoxic tent. ResultsSustained attention (RT and number of lapses in the PVT) and executive functions (Go-NoGo and 1-Back and 2-Back parameters, as inhibition and working memory signatures) were impaired in the SRHY condition compared to HSHY. SpO2 and HR were higher after 4 hours compared with 30 minutes of hypoxia in the HSHY condition, while only HR was statistically higher in the SRHY condition. In SRHY, salivary AA concentration was lower and cortisol was higher than in HSHY. A significant increase in sAA concentration is observed after the cognitive session at 4 hours of hypoxia exposure compared to that at 30 minutes, only in the SRHY condition. There are significant positive correlations between reaction time and the corresponding heart rate (a non-invasive marker of physiological stress) for the executive tasks in the two sleep conditions. This was not observed for salivary levels of sAA and cortisol, respective reliable indicators of the sympathoadrenomedullary system and the hypothalamic-pituitary adrenocortical system. ConclusionExposure to moderate normobaric hypoxia (≃ 3,500 m / ≃ 11,500 ft simulated) after a single night of 3-hour sleep impairs cognitive performance after 30 minutes and 4 hours of exposure. The key determinants and/or mechanism(s) responsible for cognitive impairment when exposed to moderate hypoxia with sleep restriction, particularly on the executive function, have yet to be elucidated.

Pathogenesis of the crosstalk between reproductive function and stress in animals-part 1: Hypothalamo-pituitary-adrenal axis, sympatho-adrenomedullary system and kisspeptin.

Stress is defined as a disruption of the body homeostasis in response to modest as well as perceived challenge. Two main physiological routes, the hypothalamic-pituitary-adrenal system (HPA) and the sympatho-adrenomedullary system (SAM), aim to maintain or restore homeostasis by mutual interaction. SAM is quickly-reacting as it primarily works through the nervous system-the sympathetic nervous system. In response to stress, signals are sent to activate the adrenal medulla which releases catecholamines (primarily adrenaline and norepinephrine). The catecholamines have a momentary effect on the body's organs that are prepared for a fight situation. At the same time, the stressor activates the HPA axis by signals from the brain causing secretion of the pituitary hormone adrenocorticotropic hormone (ACTH). ACTH acts on the adrenal cortex, which secretes glucocorticoids, including cortisol. Since HPA primarily works through hormones, the system is slightly slower than SAM and gives rise to a metabolic effect. While short-term stress response is an adaptive and beneficial process, chronic or excessive stress can lead to a range of negative health outcomes including reproductive disorders and infertility. Several mechanisms have been proposed to explain the link between stress and reproduction. This includes in particular kisspeptin, which is closely related to reproduction, as it is a powerful stimulator of the Hypothalamic-pituitary-gonadal (HPG) system. The present review, through current knowledge in various male and female species, deals with the role of the SAM and the HPA, including the major action of kisspeptin and glucocorticoids that trigger the consequences of psychological or physiological stress on reproductive function.

Pathogenesis of the crosstalk between reproductive function and stress in animals - part 2: Prolactin, thyroid, inflammation and oxidative stress.

Stress has a significant impact on reproductive health and fertility in both humans as well as various animal species. In particular, chronic stress can disrupt the delicate balance of the hormonal system that regulates reproductive function, leading to a variety of reproductive disorders and fertility issues. Beside the action of the hypothalamic-pituitary-adrenal (HPA) system and the sympatho-adrenomedullary system (SAM), other subsequent mechanisms have been incriminated. Thus, stress has also been associated with increased prolactin level, resulting in an inhibition of the hypothalamo-pituitary-gonadal (HPG) system leading to several reproductive disorders. Thyroid function is inhibited during chronic stress, and therefore considered an important regulator of reproductive function. Thus, and in particular by interfering with the HPA system, stress-induced immune dysregulation can have adverse effects on reproduction. In addition, oxidative stress and inflammation have been proposed as potential mechanisms by which chronic stress affects reproductive function. This is caused by an increase in reactive oxygen species (ROS) production that has a harmful effect on cells. Furthermore, inflammation can lead to tissue damage and scarring, which can affect fertility. The present review completes the complex mechanism linking stress and reproduction through the current knowledge in various animal species in a comparative point of view.

Effects of two mindfulness based interventions on the distinct phases of the stress response across different physiological systems

When evaluating the effects of mindfulness-based interventions (MBIs) on the stress response, several aspects should be considered, such as (1) effects on various response systems, (2) temporal dynamics of the stress response, and (3) differences between programs. This study assesses the stress-attenuating effects of a standard mindfulness-based stress reduction (MBSR) and a second-generation MBI: MBSR with elements of other Buddhist practices (MBSR-B). Ninety-nine healthy volunteers were randomly assigned to the MBSR, MBSR-B, or waitlist control groups and their stress response was evaluated with the Trier Social Stress Test. Changes in the activity of the hypothalamic-pituitary-adrenal (HPA) axis, sympathoadrenomedullary system, the autonomic nervous system (ANS), and affect were measured during distinct phases of the task. Compared to waitlist control, the stress-attenuated effects of MBIs were detected across almost all systems and both negative and positive affect. In the parasympathetic branch of the ANS, the effect of MBIs was present in all stress phases (however, in the recovery phase, only MBSR-B has shown a statistically significant effect in comparison with the waitlist control). The stress-attenuating effects of MBIs were observed already in the anticipatory phase for cortisol, ANS, and negative affect (for negative affect, only the modified MBSR-B program has shown statistically significant effect in comparison with the waitlist control).

Stimulation of brain α7-nicotinic acetylcholine receptors suppresses the rat micturition through brain GABAergic receptors

Brain nicotinic acetylcholine receptors (nAChRs) reportedly suppress the micturition, but the mechanisms responsible for this suppression remain unclear. We previously reported that intracerebroventricularly administered (±)-epibatidine (non-selective nAChR agonist) activated the sympatho-adrenomedullary system, which can affect the micturition. Therefore, we investigated (1) whether intracerebroventricularly administered (±)-epibatidine-induced effects on the micturition were dependent on the sympatho-adrenomedullary system, and (2) brain nAChR subtypes involved in the (±)-epibatidine-induced effects in urethane-anesthetized male Wistar rats. Plasma noradrenaline and adrenaline (catecholamines) were measured just before and 5 min after (±)-epibatidine administration. Evaluation of urodynamic parameters, intercontraction intervals (ICI) and maximal voiding pressure (MVP) by cystometry was started 1 h before (±)-epibatidine administration or intracerebroventricular pretreatment with other drugs and continued 1 h after (±)-epibatidine administration. Intracerebroventricularly administered (±)-epibatidine elevated plasma catecholamines and prolonged ICI without affecting MVP, and these changes were suppressed by intracerebroventricularly pretreated mecamylamine (non-selective nAChR antagonist). Acute bilateral adrenalectomy abolished the (±)-epibatidine-induced elevation of plasma catecholamines, but had no effect on the (±)-epibatidine-induced ICI prolongation. The latter was suppressed by intracerebroventricularly pretreated methyllycaconitine (selective α7-nAChR antagonist), SR95531 (GABAA antagonist), and SCH50911 (GABAB antagonist), but not by dihydro-β-erythroidine (selective α4β2-nAChR antagonist). Intracerebroventricularly administered PHA568487 (selective α7-nAChR agonist) prolonged ICI without affecting MVP, similar to (±)-epibatidine. These results suggest that stimulation of brain α7-nAChRs suppresses the rat micturition through brain GABAA/GABAB receptors, independently of the sympatho-adrenomedullary outflow modulation.

Differential Responses of Urinary Epinephrine and Norepinephrine to 24-h Shift-Work Stressor in Physicians.

Multiple stressors, including 24-h-shifts characterise the working environment of physicians, influencing well-being, health and performance. We aimed to evaluate the effect of the stressor 24-h-shift on the adrenal medullary and sympathoneural system in physicians with the hypothesis that shift work might have different impacts on both systems. Twenty-two physicians collected two 12-h-urine samples (“daytime” and “nighttime”) during a 24-h shift (“on-duty”) and on a free weekend (“off-duty”), respectively. Urinary excretion rates per m2 body surface area were assessed for the catecholamines epinephrine, norepinephrine and their respective free O-methylated metabolites metanephrine and normetanephrine by LC-MS/MS-analysis. The stressor provoked differential responses of epinephrine and norepinephrine. Epinephrine excretion rates showed significant increases from off to on duty. The largest proportional change (off-duty to on-duty) for epinephrine was observed for nighttime (205%), the increase for daytime was 84%. An increase in norepinephrine from off to on duty was only visible for nighttime collections. For the catecholamine metabolites, normetanephrine paralleled norepinephrine and exhibited an increase in excretion from off to on duty during nighttime collections of 53% whereas there was no change during daytime collections (3%). In conclusion: Whilst the 24-h-shift-work stressor in physicians activates the sympatho-adrenomedullary system, represented by epinephrine, the sympathoneural response through norepinephrine reflects mainly an ambulatory position during working hours.

Brain nitric oxide induces facilitation of the micturition reflex through brain glutamatergic receptors in rats.

Brain nitric oxide (NO) have been reported in regulation of the sympatho-adrenomedullary system, which can affect voiding and storage functions. Therefore, we investigated effects of intracerebroventricularly (icv) administered 3-(4-morpholinyl)sydnonimine, hydrochloride (SIN-1) (NO donor) on the micturition reflex, focusing on their dependence on the sympatho-adrenomedullary system and on brain N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors in urethane-anesthetized (0.8 g/kg, ip) male Wistar rats. Plasma noradrenaline and adrenaline were measured just before and 5 minutes after SIN-1 administration. Evaluation of urodynamic parameters was started 1 hour before SIN-1 administration or intracerebroventricular pretreatment with other drugs. SIN-1 (100 and 250 µg/animal) elevated plasma adrenaline and reduced intercontraction interval([ICI]values; 110.5% [SIN-1, 0 µg]and 54.9% [SIN-1, 250 µg]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.59]) without affecting plasma noradrenaline or maximal voiding pressure. SIN-1 (250 µg/animal) reduced single-voided volume and bladder capacity without affecting post-voiding residual volume. The SIN-1 (250 µg/animal)-induced adrenaline elevation and ICI reduction were attenuated by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, sodium salt (carboxy-PTIO) (NO scavenger, icv) (ICI values; 44.7% [vehicle + SIN-1]and 77.5% [carboxy-PTIO + SIN-1]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.51]). Acute bilateral adrenalectomyabolished SIN-1-induced adrenaline elevation, while showed no effect on the SIN-1-induced ICI reduction. The ICI reduction was attenuated by MK-801 (NMDA receptor antagonist, icv) (ICI values; 47.0% [vehicle + SIN-1]and 87.6% [MK-801 + SIN-1]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.61]), but not by DNQX (AMPA receptor antagonist, icv). Brain NO is involved in facilitation of the rat micturition reflex through brain NMDA receptors, independently of the sympatho-adrenomedullary outflow modulation.

Stimulation of brain cannabinoid CB1 receptors can ameliorate hypertension in spontaneously hypertensive rats.

Excessive activation of the sympatho-adrenomedullary system plays a pathogenic role in triggering and sustaining essential hypertension. We previously reported that, in normotensive rats, intracerebroventricularly (i.c.v.) administered neuropeptides, corticotropin-releasing factor and bombesin induced activation of the sympatho-adrenomedullary system, and that brain cannabinoid CB1 receptors negatively regulated this activation. In this study, we investigated the effects of brain CB1 receptor stimulation on blood pressure and the sympatho-adrenomedullary outflow in spontaneously hypertensive rats (SHRs), commonly used animal models of essential hypertension, and in Wistar-Kyoto (WKY) rats, normotensive controls of SHRs. In 18-week-old SHRs and WKY rats under urethane anaesthesia (1.0g/kg, i.p.), SHRs exhibited significantly higher systolic, mean and diastolic blood pressures and plasma noradrenaline and adrenaline, and a lower heart rate than WKY rats. Single administration of arachidonyl 2'-chloroethylamide (ACEA, CB1 agonist, 1.4µmol/animal, i.c.v.) significantly but partially reduced mean and diastolic blood pressures and the plasma level of noradrenaline in SHRs compared to vehicle (N,N-dimethylformamide)-treated SHRs. These ACEA-induced reductions were abolished by central pretreatment with rimonabant (CB1 antagonist, 300nmol/animal, i.c.v.), which alone showed no significant effect on blood pressures or plasma noradrenaline and adrenaline levels of SHRs. On the other hand, ACEA had no significant effect on blood pressure or plasma noradrenaline and adrenaline levels in WKY rats. These results suggest that stimulation of brain CB1 receptors can ameliorate hypertension accompanied by enhanced sympathetic outflow without affecting blood pressure under normotensive conditions.

Haplotypes of coping behavior associated QTL regions reveal distinct transcript profiles in amygdala and hippocampus

Stress response and coping behavior in pigs are largely shaped by hypothalamic-pituitary-adrenal axis and sympatho-adrenomedullary system action. However, the dynamic interaction between amygdala and hippocampus crucially modulates the behavioral response towards significant emotional events. While this functional relationship is well documented, the molecular underpinnings still remain insufficiently understood. Our study used transcriptome profiling of porcine amygdala and hippocampus to identify molecular pathways that are differentially activated depending on the haplotype of a significantly coping behavior-associated region on pig chromosome 12 (SSC12). The pigs were classified into two groups based on the haplotype information of this QTL-region discovered in our previous genome-wide association study. Ten each of high- (HR) and low- (LR) reactive pigs (n = 20) were selected for differential gene expression analysis and weighted gene co-expression analysis with subsequent pathway analysis. Differentially expressed genes identified in the amygdala include SELL, CXCR7 and NTS, while TRAF3, PTGS2 and CFI were detected in the hippocampus indicating a role of neuroinflammation and immunological processes. Pathway analysis revealed IL-8 signaling, NF-κB signaling, glutamate and GABA metabolism, glucocorticoid receptor signaling and chemokine signaling in the amygdala and ephrin receptor signaling, as well as NF-κB signaling in the hippocampus. We discovered candidate genes in regions detected by genome-wide association study including ARRB2, ADRBK2, THRB, NEK7 and ACVR2B, which relate to dopaminergic and other monoaminergic neurotransmitter systems, neuroimmunomodulation, neuroinflammation and GABA-ergic neurotransmission. These findings provide insights into the molecular underpinning of divergent coping behavior and associated haplotypes in limbic forebrain system in pig.

Neurobiology and consequences of social isolation stress in animal model—A comprehensive review

The brain is a vital organ, susceptible to alterations under genetic influences and environmental experiences. Social isolation (SI) acts as a stressor which results in alterations in reactivity to stress, social behavior, function of neurochemical and neuroendocrine system, physiological, anatomical and behavioral changes in both animal and humans. During early stages of life, acute or chronic SIS has been proposed to show signs and symptoms of psychiatric and neurological disorders such as anxiety, depression, schizophrenia, epilepsy and memory loss. Exposure to social isolation stress induces a variety of endocrinological changes including the activation of hypothalamic-pituitary-adrenal (HPA) axis, culminating in the release of glucocorticoids (GCs), release of catecholamines, activation of the sympatho-adrenomedullary system, release of Oxytocin and vasopressin. In several regions of the central nervous system (CNS), SIS alters the level of neurotransmitter such as dopamine, serotonin, gamma aminobutyric acid (GABA), glutamate, nitrergic system and adrenaline as well as leads to alteration in receptor sensitivity of N-methyl-D-aspartate (NMDA) and opioid system. A change in the function of oxidative and nitrosative stress (O&NS) mediated mitochondrial dysfunction, inflammatory factors, neurotrophins and neurotrophicfactors (NTFs), early growth response transcription factor genes (Egr) and C-Fos expression are also involved as a pathophysiological consequences of SIS which induce neurological and psychiatric disorders.

Hyperactivity of the Sympatho-Adrenomedullary System Without Any Modification of the Hypothalamic-Pituitary-Adrenal Axis After Food Restriction Among High-Level Weightlifters.

Durguerian, A, Filaire, E, Drogou, C, Sauvet, F, Bougard, C, and Chennaoui, M. Hyperactivity of the sympatho-adrenomedullary system without any modification of the hypothalamic-pituitary-adrenal axis after food restriction among high-level weightlifters. J Strength Cond Res 32(6): 1643-1655, 2018-We examined the effects of 6 days of food restriction on salivary α-amylase (sAA), cortisol and dehydroepiandrostenedione (DHEA) awakening responses, psychological parameters and performance among 11 international weightlifters. Assessments were made at baseline (T1) and 6 days after a normal period of training while maintaining body weight (T2). Then, participants were assigned to 2 groups depending on whether they lost (Diet group) or maintained (Control group) their body mass. Anthropometric, psychological, physical, and physiological assessments were also realized 6 days (T3) after the restricted dietary period for the Diet group. Food restriction (T3) induced a significant rise of sAA awakening response (364.6%, p ≤ 0.05), whereas no significant variations were observed among the hypothalamic-pituitary-adrenal axis (cortisol and DHEA). Significant alterations of the general Recovery Score and General stress Score, evaluated through the Recovery-Stress Questionnaire for athletes, were noted after food restriction. Weightlifting performance, evaluated during a simulated weightlifting competition, was maintained after the 6-day food restriction; we even noted an increased weightlifting performance related to body mass (Sinclair coefficient). Our findings support the hypothesis that food restriction induces a challenging situation to the organism, resulting in an asymmetry between the 2 stress systems activation. These results reinforce the necessity to cautiously plan and monitor the weight regulation process before competition to avoid potential negative outcomes on psychophysiological parameters. In this regard, the psychobiological approach, especially the awakening responses, seems a useful tool.

MP09-09 BRAIN NITRIC OXIDE CAN INDUCE FREQUENT URINATION IN RATS

You have accessJournal of UrologyBladder & Urethra: Anatomy, Physiology & Pharmacology I1 Apr 2018MP09-09 BRAIN NITRIC OXIDE CAN INDUCE FREQUENT URINATION IN RATS Takahiro Shimizu, Hideaki Ono, Shogo Shimizu, Youichirou Higashi, Suo Zou, Masaki Yamamoto, Takaaki Aratake, Tomoya Hamada, Yoshiki Nagao, Yusuke Ueba, Masashi Honda, and Motoaki Saito Takahiro ShimizuTakahiro Shimizu More articles by this author , Hideaki OnoHideaki Ono More articles by this author , Shogo ShimizuShogo Shimizu More articles by this author , Youichirou HigashiYouichirou Higashi More articles by this author , Suo ZouSuo Zou More articles by this author , Masaki YamamotoMasaki Yamamoto More articles by this author , Takaaki AratakeTakaaki Aratake More articles by this author , Tomoya HamadaTomoya Hamada More articles by this author , Yoshiki NagaoYoshiki Nagao More articles by this author , Yusuke UebaYusuke Ueba More articles by this author , Masashi HondaMasashi Honda More articles by this author , and Motoaki SaitoMotoaki Saito More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2018.02.335AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Nitric oxide (NO) has a local inhibitory effect on urination. While in the central nervous system, NO seems to have both inhibitory and facilitatory effects on micturition. We previously reported that an NO donor SIN-1 centrally activated the sympatho-adrenomedullary (SA) system in rats. In this study, we investigated effects of centrally administered SIN-1 on micturition and their dependence on the SA system in rats. METHODS Urethane anesthetized (0.8-1.0 g/kg, ip) male Wistar rats (300-400 g) were used. (1) Catheters were inserted into the bladder and the femoral artery in order to perform continuous cystometrograms (CMG, 12 ml/h saline infusion) and to collect blood samples, respectively. Three hours after the surgery, SIN-1 (100 or 250 μg/rat) or vehicle was icv administered. Saline infusion into the bladder was started 1 hour before the icv administration. Plasma noradrenaline (NA) and adrenaline (Ad) levels were measured at 5 min after the icv administration. In some experiments, carboxy-PTIO (PTIO, an NO scavenger, 750 μg/rat) was icv pretreated 30 min before icv SIN-1 administration. (2) Three hours after the surgery of a bladder catheter insertion, single CMG (12 ml/h saline infusion) was performed. After 4-5 times of single CMG, SIN-1 (250 μg/rat) was icv administered, then single CMG was continued for 1 hour. RESULTS (1) SIN-1 dose-dependently reduced intercontraction intervals (ICI) and elevated plasma Ad without altering maximal voiding pressure or plasma NA (Tables 1-2). An insufficient dose of SIN-1 (100 μg/rat) for elevating plasma AD could induce ICI reduction (Tables 1-2). These SIN-1-induced responses were inhibited by PTIO (Table 3). (2) SIN-1 reduced single-voided volume (Vv) and bladder capacity (BC) without altering post-voiding residual urine volume or voiding efficiency (Table 4). CONCLUSIONS NO centrally induces frequent urination shown by reduced ICI, Vv and BC, independent of the central SA outflow. Thus, the brain nitrergic pathway that is directly involved in the control of micturition could be a new target for the treatment of bladder dysfunction. © 2018FiguresReferencesRelatedDetails Volume 199Issue 4SApril 2018Page: e109 Advertisement Copyright & Permissions© 2018MetricsAuthor Information Takahiro Shimizu More articles by this author Hideaki Ono More articles by this author Shogo Shimizu More articles by this author Youichirou Higashi More articles by this author Suo Zou More articles by this author Masaki Yamamoto More articles by this author Takaaki Aratake More articles by this author Tomoya Hamada More articles by this author Yoshiki Nagao More articles by this author Yusuke Ueba More articles by this author Masashi Honda More articles by this author Motoaki Saito More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Elevated biomarkers of sympatho-adrenomedullary activity linked to e-waste air pollutant exposure in preschool children

Air pollution is a risk factor for cardiovascular disease (CVD), and cardiovascular regulatory changes in childhood contribute to the development and progression of cardiovascular events at older ages. The aim of the study was to investigate the effect of air pollutant exposure on the child sympatho-adrenomedullary (SAM) system, which plays a vital role in regulating and controlling the cardiovascular system. Two plasma biomarkers (plasma epinephrine and norepinephrine) of SAM activity and heart rate were measured in preschool children (n = 228) living in Guiyu, and native (n = 104) and non-native children (n = 91) living in a reference area (Haojiang) for >1 year. Air pollution data, over the 4-months before the health examination, was also collected. Environmental PM2.5, PM10, SO2, NO2 and CO, plasma norepinephrine and heart rate of the e-waste recycling area were significantly higher than for the non-e-waste recycling area. However, there was no difference in plasma norepinephrine and heart rate between native children living in the non-e-waste recycling area and non-native children living in the non-e-waste recycling area. PM2.5, PM10, SO2 and NO2 data, over the 30-day and the 4-month average of pollution before the health examination, showed a positive association with plasma norepinephrine level. PM2.5, PM10, SO2, NO2 and CO concentrations, over the 24 h of the day of the health examination, the 3 previous 24-hour periods before the health examination, and the 24 h after the health examination, were related to increase in heart rate. At the same time, plasma norepinephrine and heart rate on children in the high air pollution level group (≤50-m radius of family-run workshops) were higher than those in the low air pollution level group. Our results suggest that air pollution exposure in e-waste recycling areas could result in an increase in heart rate and plasma norepinephrine, implying e-waste air pollutant exposure impairs the SAM system in children.

The Role of the Sympathoadrenomedullary System in the Formation of Pilot’s Adaptation to Flight Loads

The objective of this study was to evaluate the functions of the sympathoadrenomedullary system and the related psychophysiological reactions of pilots, depending on flying hours on a highly maneuverable aircraft. The study involved 78 volunteer pilots (41 high-maneuverability pilots and 37 bomber and transport aviation pilots). A set of methods was chosen with the possibility of their use according to the principle of comprehensive evaluation of the body functional state under flight loads taken into account. Our results indicate that highly maneuverable aircraft piloting induces a significant activation of the sympathoadrenomedullary system in pilots, compared to bombing and transport aircrafts. This is particularly common to young pilots with the total flying time of less than 1000 h. It has been recorded that changes in adaptation to the effect of flight factors on the body develop with age and flight experience.

Angiotensin II centrally induces frequent detrusor contractility of the bladder by acting on brain angiotensin II type 1 receptors in rats.

Angiotensin (Ang) II plays an important role in the brain as a neurotransmitter and is involved in psychological stress reactions, for example through activation of the sympatho-adrenomedullary system. We investigated the effects of centrally administered Ang II on the micturition reflex, which is potentially affected by the sympatho-adrenomedullary system, and brain Ang II receptors in urethane-anesthetized (1.0 g/kg, intraperitoneally) male rats. Central administration of Ang II (0.01, 0.02, and 0.07 nmol per rat, intracerebroventricularly, icv) but not vehicle rapidly and dose-dependently decreased the urinary bladder intercontraction interval, without altering the bladder detrusor pressure. Central administration of antagonists of Ang II type 1 but not type 2 receptors inhibited the Ang II-induced shortening of intercontraction intervals. Administration of the highest dose of Ang II (0.07 nmol per rat, icv) but not lower doses (0.01 and 0.02 nmol per rat, icv) elevated the plasma concentration of adrenaline. Bilateral adrenalectomy reduced Ang II-induced elevation in adrenaline, but had no effect on the Ang II-induced shortening of the intercontraction interval. These data suggest that central administration of Ang II increases urinary frequency by acting on brain Ang II type 1 receptors, independent of activation of the sympatho-adrenomedullary system.

A Stress-Related Peptide Bombesin Centrally Induces Frequent Urination through Brain Bombesin Receptor Types 1 and 2 in the Rat.

Stress exacerbates symptoms of bladder dysfunction including overactive bladder and bladder pain syndrome, but the underlying mechanisms are unknown. Bombesin-like peptides and bombesin receptor types 1 and 2 (BB1 and BB2, respectively) in the brain have been implicated in the mediation/integration of stress responses. In this study, we examined effects of centrally administered bombesin on micturition, focusing on their dependence on 1) the sympathoadrenomedullary system (a representative mechanism activated by stress exposure) and 2) brain BB receptors in urethane-anesthetized (1.0-1.2 g/kg, i.p.) male rats. Intracerebroventricularly administered bombesin significantly shortened intercontraction intervals (ICI) at both doses (0.1 and 1 nmol/animal) without affecting maximal voiding pressure. Bombesin at 1 nmol induced significant increments of plasma noradrenaline and adrenaline levels, which were both abolished by acute bilateral adrenalectomy. On the other hand, adrenalectomy showed no effects on the bombesin-induced shortening of ICI. Much lower doses of bombesin (0.01 and 0.03 nmol/animal, i.c.v.) dose-dependently shortened ICI. Pretreatment with either a BB1 receptor antagonist (BIM-23127; d-Nal-cyclo[Cys-Tyr-d-Trp-Orn-Val-Cys]-Nal-NH2; 3 nmol/animal, i.c.v.) or a BB2 receptor antagonist (BEA; H-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt; 3 nmol/animal, i.c.v.), respectively, suppressed the BB (0.03 nmol/animal, i.c.v.)-induced shortening of ICI, whereas each antagonist by itself (1 and 3 nmol/animal, i.c.v.) had no significant effects on ICI. Bombesin (0.03 nmol/animal, i.c.v.) significantly reduced voided volume per micturition and bladder capacity without affecting postvoid residual volume or voiding efficiency. These results suggest that brain bombesin and BB receptors are involved in facilitation of the rat micturition reflex to induce bladder overactivity, which is independent of the sympathoadrenomedullary outflow modulation.

Brain opioid and nociceptin receptors are involved in regulation of bombesin-induced activation of central sympatho-adrenomedullary outflow in the rat

Previously, we reported that central administration of bombesin, a stress-related peptide, elevated plasma levels of catecholamines (noradrenaline and adrenaline) in the rat. The sympatho-adrenomedullary system, which is an important component of stress responses, can be regulated by the central opioid system. In the present study, therefore, we examined the roles of brain opioid receptor subtypes (µ, δ, and κ) and nociceptin receptors, originally identified as opioid-like orphan receptors, in the bombesin-induced activation of central sympatho-adrenomedullary outflow using anesthetized male Wistar rats. Intracerebroventricularly (i.c.v.) administered bombesin-(1nmol/animal) induced elevation of plasma catecholamines was significantly potentiated by pretreatment with naloxone (300 and 1000µg/animal, i.c.v.), a non-selective antagonist for µ-, δ-, and κ-opioid receptors. Pretreatment with cyprodime (100µg/animal, i.c.v.), a selective antagonist for µ-opioid receptors, also potentiated the bombesin-induced responses. In contrast, pretreatment with naltrindole (100µg/animal, i.c.v.) or nor-binaltorphimine (100µg/animal, i.c.v.), a selective antagonist for δ- or κ-opioid receptors, significantly reduced the elevation of bombesin-induced catecholamines. In addition, pretreatment with JTC-801 (30 and 100µg/animal, i.c.v.) or J-113397 (100µg/animal, i.c.v.), which are selective antagonists for nociceptin receptors, also reduced the bombesin-induced responses. These results suggest that brain µ-opioid receptors play a suppressive role and that brain δ-, κ-opioid, and nociceptin receptors play a facilitative role in the bombesin-induced elevation of plasma catecholamines in the rat. Thus, in the brain, these receptors could play differential roles in regulating the activation of central sympatho-adrenomedullary outflow.

Retrieval-induced forgetting under psychosocial stress: No reduction by delayed stress and beta-adrenergic blockade

Retrieval-induced forgetting (RIF) is the phenomenon that ‘retrieval-practice’, the repeated retrieval of a subset of initially learned material, can impair the recall of episodically related memories. Previous studies showed that RIF is eliminated when retrieval-practice is carried out under psycho-social stress, anxiety, or in negative mood. However, pharmacological manipulation by hydrocortisone did not eliminate the effect. This study investigated the effect of beta-adrenergic blockade on stress-induced modulations of RIF, addressing possible interactive effects of the glucocorticoid and sympatho–adrenomedullary systems. Participants learned categorized word lists and then received either 60mg propranolol or a placebo. After 90min they were exposed to the TSST. A third group did not receive any medication and performed a non-stressful control task with the same timing as the other two groups. Finally, all participants underwent retrieval-practice and final recall. Both TSST groups exhibited a stress-induced increase in cortisol-levels, and the placebo group also exhibited large increases in markers of sympathetic nervous system activity and more psychological distress at the time of retrieval-practice. Although, overall recall was poorer under stress, an overall RIF effect emerged irrespective of group and showed no clear modulation by stress with or without beta-adrenergic blockade. In previous demonstrations of RIF elimination by negative emotion, state induction and retrieval-practice followed very briefly after initial learning. Given that both the previous study of hydrocortisone effects on RIF and the present study used longer delays between learning and retrieval-practice, the possibility that stress effects on retrieval-practice eliminate RIF only relatively briefly after learning is discussed.

Saliva chromogranin A in growing pigs: A study of circadian patterns during daytime and stability under different storage conditions

Salivary chromogranin A (CgA) is considered to be a biomarker of activation of the sympatho-adrenomedullary system, and has recently been proposed as a useful indicator of the acute stress response in pigs. The aim of the present study was to determinate whether salivary CgA concentrations in healthy growing pigs exhibits any circadian pattern during the daytime, and to evaluate its stability under different storage conditions. A total of 80 pigs (40 in spring and another 40 in autumn) of two different ages and genders were used. To establish the circadian pattern, saliva samples were collected at 07.00, 11.00, 15.00 and 19.00h on two consecutive days. Pooled samples were used for the stability study and were measured on the day of sampling and periodically for up to 360days later. Samples were stored at 4°C, −20°C or −80°C and the effect of repeated freezing and thawing was also evaluated.No circadian pattern was detected for salivary CgA in either season and there were no significant effects of gender or age. However, mean salivary CgA concentrations were significantly higher (P<0.0001) in the pigs sampled in autumn, compared to those sampled in the spring. Short term storage at 4°C is recommended for up to 2days, whereas frozen samples can be stored for 1year at −20°C or −80°C, without substantial reduction in CgA values. In addition, samples can be frozen and thawed up to seven times without significant loss of the biomarker.

Salivary cortisol levels, but not salivary α‐amylase levels, are elevated in patients with rheumatoid arthritis irrespective of depression

Stress is recognized as an important factor in the etiology of rheumatoid arthritis (RA). Therefore, we explored multiple aspects of stress in RA patients. Salivary cortisol and α-amylase levels were measured as markers of the hypothalamic-pituitary-adrenal axis activity and sympatho-adrenomedullary system activity, respectively. Depression was assessed by the Beck Depression Inventory (BDI) and short-term analysis of the heart rate variability (HRV) was performed to evaluate the autonomic nervous system. The salivary cortisol levels of the RA patients were significantly higher than those of the normal controls (NC; 0.12±0.162μg/dL vs. 0.068±0.052μg/dL, P=0.006). There was no difference in salivary α-amylase levels between the RA and the NC. The BDI levels of the RA patients were significantly higher than the NC (13.7±8.9 vs. 6.4±6.9, P<0.001). Depression was more prevalent in RA patients than in the NC. The salivary cortisol levels were still significantly higher in the RA than the NC after controlling BDI by logistic regression analysis (P=0.002). There was no significant difference in the HRV of RA patients and the NC. The evaluation of relationship between stress measures and disease activity markers of RA revealed that only BDI was positively correlated with the visual analogue pain scale. Salivary cortisol levels and the BDI of RA patients were higher than those of the NC, and elevated salivary cortisol levels were independent of depression. However, the level of stress may not be correlated with disease activity in RA.