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Journal articles on the topic 'Adrenergic stress'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Wong, Dona L., T. C. Tai, David C. Wong-Faull, Robert Claycomb, and Richard Kvet��ansk��. "Adrenergic Responses to Stress." Annals of the New York Academy of Sciences 1148, no. 1 (2008): 249–56. http://dx.doi.org/10.1196/annals.1410.048.

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2

Nakamori, T., A. Morimoto, K. Morimoto, N. Tan, and N. Murakami. "Effects of alpha- and beta-adrenergic antagonists on rise in body temperature induced by psychological stress in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 1 (1993): R156—R161. http://dx.doi.org/10.1152/ajpregu.1993.264.1.r156.

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We investigated the effects of intraperitoneal injection of alpha- and beta-adrenergic antagonists on psychological stress-induced responses in free-moving rats. Psychological stress was induced by immersion in 2-cm-deep water. The intraperitoneal injection of the alpha-adrenergic blocker, phentolamine (10 mg/kg), attenuated the stress-induced rise in body temperature and hypertension but enhanced tachycardia. In contrast, intraperitoneal injection of the beta-adrenergic blocker, propranolol (1 mg/kg), suppressed tachycardia but had no effect on rise in body temperature and hypertension during

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3

Haustein, U. F. "Adrenergic urticaria and adrenergic pruritus." Acta Dermato-Venereologica 70, no. 1 (1990): 82–84. http://dx.doi.org/10.2340/00015555708284.

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We report here on 2 patients with adrenergic urticaria and adrenergic pruritus, respectively. The lesions and features developed during phases of stress and during the attacks were associated with an increase in the plasma concentrations of noradrenalin, adrenalin and prolactin. The dopamine plasma level was elevated only in the case of adrenergic urticaria. The symptoms could be reproduced by intradermal injection of adrenalin and noradrenalin and treated successfully with propanolol, a blocker of beta-adrenergic receptors. Adrenergic urticaria is a rare but distinct entity, which has to be s

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4

Suleymanoglu, Yilmaz, Dimitar Bakalov, Zafer Sabit, Vlayko Vodenicharov, Radka Tafradjiiska-Hadjiolova, and Hristina Nocheva. "The endogenous cannabinoid and the adrenergic systems in modulation of stress-response." Pharmacia 71, no. () (2024): 1–8. https://doi.org/10.3897/pharmacia.71.e115659.

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In our modern, fast-paced society, excessive stress (or distress) is a major risk factor for developing a plethora of diseases. There are several neuromediatory systems in the brain that regulate the response to stress, including the adrenergic and endocannabinoid systems. In our experiments, we study the effects of the endocannabinoid system on the restrain stress-induced analgesia (r-SIA). The experiments were done on male Wistar rats. The animals were confined in special restrainers for a period of one hour. The animals were treated with Clonidine (at 4 mg/kg) – a prototypical α2-agonist; Y

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5

Bryan, R. M. "Cerebral blood flow and energy metabolism during stress." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 2 (1990): H269—H280. http://dx.doi.org/10.1152/ajpheart.1990.259.2.h269.

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Many, but not all, stressful events are accompanied by increases in cerebral blood flow and/or energy metabolism. The stressful events include pharmacological paralysis, footshock, conditioned fear, hypotension, hypoglycemia, hypoxia, noise, and ethanol withdrawal. These increases are significant because 1) all brain regions are often affected, i.e., certain stressful events have global effects on cerebral blood flow and energy metabolism; and 2) various stressful events appear to have a common adrenergic mechanism for increasing cerebral blood flow and energy metabolism. The adrenergic mechan

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6

Okajima, Masaki, Masayuki Takamura, Philippe Véquaud, Robert Parent та Michel Lavallée. "β-Adrenergic receptor blockade impairs NO-dependent dilation of large coronary arteries during exercise". American Journal of Physiology-Heart and Circulatory Physiology 284, № 2 (2003): H501—H510. http://dx.doi.org/10.1152/ajpheart.00419.2002.

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Shear stress-dependent nitric oxide (NO) formation prevents immoderate vascular constriction. We examined whether shear stress-dependent NO formation limits exercise-induced coronary artery constriction after β-adrenergic receptor blockade in dogs. Control exercise led to increases ( P < 0.01) in coronary blood flow (CBF) by 38 ± 5 ml/min from 41 ± 5 ml/min and in the external diameter of epicardial coronary arteries (CD) by 0.24 ± 0.03 mm from 3.33 ± 0.20 mm. CD and shear stress were linearly related. After propranolol, CD fell ( P < 0.01) during exercise (0.08 ± 0.03 from 3.23 ± 0.19 m

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7

Maloyan, Alina, та Michal Horowitz. "β-Adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation". Journal of Applied Physiology 93, № 1 (2002): 107–15. http://dx.doi.org/10.1152/japplphysiol.01122.2001.

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Heat acclimation upregulates 72-kDa heat shock protein (HSP72) and predisposes to faster activation of the heat shock response (HSR). This study investigates the role played by β-adrenergic signaling and/or plasma thyroxine level in eliciting these features by using rats undergoing 1) heat acclimation (AC; 34°C, 2 and 30 days); 2) AC with β-adrenergic blockade; 3) AC-maintained euthyroid; 4) hypothyroid; 5) hyperthyroid; and 6) controls. The hsp72 mRNA (RT-PCR) and HSP72 levels (Western blot) were measured before and after heat stress (2 h, 41°C, rectal temperature monitored). β-Adrenergic blo

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8

Perry, S., S. Reid, and A. Salama. "The effects of repeated physical stress on the b-adrenergic response of the rainbow trout red blood cell." Journal of Experimental Biology 199, no. 3 (1996): 549–62. http://dx.doi.org/10.1242/jeb.199.3.549.

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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

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9

Qiao, Guanxi, Mark J. Bucsek, Bonnie L. Hylander, and Elizabeth A. Repasky. "Adrenergic signaling impairs activation of CD8+ T cells by blocking metabolic reprogramming." Journal of Immunology 198, no. 1_Supplement (2017): 76.27. http://dx.doi.org/10.4049/jimmunol.198.supp.76.27.

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Abstract Adrenergic stress promotes tumor progression by several mechanisms. Mice housed at standard housing temperature (ST, 22°C) experience chronic adrenergic cold stress sufficient to elevate norepinephrine levels compared to mice housed at thermoneutrality (TT, 30°C) and we found that tumors grow faster at ST. We have also previously reported that the anti-tumor immune response is suppressed at ST. Tumor infiltrating CD8+ T cells from these mice have reduced expression of activation and effector function markers. These deficits are reversed by housing mice at TT which reduced adrenergic s

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10

Nocheva, Hristina Hristova, Eleonora Nikolaeva Encheva-Stoykova, and Evgeni Evgeniev Grigorov. "Interaction between endocannabinoids and the adrenergic system before and after stress-exposure." Pharmacia 69, no. 1 (2022): 249–54. http://dx.doi.org/10.3897/pharmacia.69.e80550.

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Cold stress-induced analgesia (c-SIA) has been evaluated in male Wistar rats injected with cannabinoid receptors type 1 and a2-adrenergic receptor agonists and antagonists in different combinations before or after stress exposure. The aim of the study was to evaluate whether the endogenous cannabinoid and the adrenergic systems influenced c-SIA, and the patterns of their potential interaction. Exogenous administration of anandamide and Clonidine together, before or after stress exposure, increased c-SIA even with differences in the time of manifestation of the effect, its duration and the degr

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11

Pearson, Mike, Glen Van Der Kraak, and E. Don Stevens. "In vivo pharmacology of spleen contraction in rainbow trout." Canadian Journal of Zoology 70, no. 3 (1992): 625–27. http://dx.doi.org/10.1139/z92-091.

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Rainbow trout, Oncorhynchus mykiss, were injected with an adrenergic agonist, an adrenergic antagonist, or a cholinergic antagonist, via a dorsal aorta cannula. Spleen size and haemoglobin content were measured at rest and, for antagonists, following an air exposure stress. Injection of phentolamine (an α-antagonist) blocked the spleen contraction induced by air exposure, suggesting that control is mediated by α-adrenergic receptors. Air exposure effects were unaffected by β-adrenergic blockade or muscarinic cholinergic blockade.

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12

Botten, Giovanni, Philip Scumpia, Kevin Doty, and Stephen Smale. "Global regulation of Toll-like receptor 4-induced inflammatory gene networks by physiologic stress signals in macrophages (INM7P.356)." Journal of Immunology 194, no. 1_Supplement (2015): 194.13. http://dx.doi.org/10.4049/jimmunol.194.supp.194.13.

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Abstract Physiologic stress mediated through adrenergic (catecholamines) and neuroendocrine (glucocorticoids) signals negatively impacts cutaneous host defense to pathogens and worsens inflammatory skin conditions such as psoriasis. Toll-like receptors (TLRs) on macrophages and other innate immune cells sense danger signals and trigger innate and adaptive immunity, but whether these stress stimuli affect similar or exclusive TLR-dependent immune pathways is unclear. We hypothesize that quantitative analysis by RNAseq will provide critical information into the mechanism by which stress affects

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13

Nocheva, Hristina Hristova, Eleonora Nikolaeva Encheva-Stoykova, and Evgeni Evgeniev Grigorov. "Interaction between endocannabinoids and the adrenergic system before and after stress-exposure." Pharmacia 69, no. (1) (2022): 249–54. https://doi.org/10.3897/pharmacia.69.e80550.

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Cold stress-induced analgesia (c-SIA) has been evaluated in male Wistar rats injected with cannabinoid receptors type 1 and a<sub>2</sub>-adrenergic receptor agonists and antagonists in different combinations before or after stress exposure. The aim of the study was to evaluate whether the endogenous cannabinoid and the adrenergic systems influenced c-SIA, and the patterns of their potential interaction. Exogenous administration of anandamide and Clonidine together, before or after stress exposure, increased c-SIA even with differences in the time of manifestation of the effect, its duration a

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14

Sari, Dwi Cahyani Ratna, Wiwit Ananda Wahyu Setyaningsih, Rizky Nur Mainichi, et al. "Centella Asiatica (GOTU KOLA) TREATMENT ATTENUATES PRO-INFLAMMATORY MEDIATORS IN LIVER OF RATS WITH ELECTRICAL FOOT SHOCK STRESS MODEL." African Journal of Traditional, Complementary and Alternative Medicines 17, no. 2 (2020): 1–7. http://dx.doi.org/10.21010/ajtcam.v17i2.1.

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Background: Stress induces secretion of cathecolamines and glucocorticoids, which may produce liver injury. Followed by the production of inflammatory mediators, it causes apoptosis. Centella asiatica (CeA) has anti-inflammatory and hepatoprotective effects. The present study aims to determine the role of CeA in the attenuation of liver pro-inflammatory mediator expression in rats with electrical foot shock stress model. Materials and Methods: Twenty-four Sprague-Dawley rats were randomized into four groups consisted of six rats each: (1) Control group, (2) CeA-treated group, (3) Stress group,

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Sari, Dwi Cahyani Ratna, Wiwit Ananda Wahyu Setyaningsih, Rizky Nur Mainichi, et al. "Centella Asiatica (GOTU KOLA) TREATMENT ATTENUATES PRO-INFLAMMATORY MEDIATORS IN LIVER OF RATS WITH ELECTRICAL FOOT SHOCK STRESS MODEL." African Journal of Traditional, Complementary and Alternative Medicines 17, no. 2 (2023): 1–7. http://dx.doi.org/10.21010/ajtcamv17i2.1.

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Background: Stress induces secretion of cathecolamines and glucocorticoids, which may produce liver injury. Followed by the production of inflammatory mediators, it causes apoptosis. Centella asiatica (CeA) has anti-inflammatory and hepatoprotective effects. The present study aims to determine the role of CeA in the attenuation of liver pro-inflammatory mediator expression in rats with electrical foot shock stress model. Materials and Methods: Twenty-four Sprague-Dawley rats were randomized into four groups consisted of six rats each: (1) Control group, (2) CeA-treated group, (3) Stress group,

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16

A.JONES, C., L. J. WILKINS, A. J. WEBB та N. G. GREGORY. "β-adrenergic responsiveness in stress-sensitive and stress-resistant pigs". Journal of Veterinary Pharmacology and Therapeutics 12, № 1 (1989): 14–18. http://dx.doi.org/10.1111/j.1365-2885.1989.tb00635.x.

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17

Pérez, Cristina, Rubén Cebollada, Konstantinos A. Mountris, Juan Pablo Martínez, Pablo Laguna та Esther Pueyo. "The role of β-adrenergic stimulation in QT interval adaptation to heart rate during stress test". PLOS ONE 18, № 1 (2023): e0280901. http://dx.doi.org/10.1371/journal.pone.0280901.

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The adaptation lag of the QT interval after heart rate (HR) has been proposed as an arrhythmic risk marker. Most studies have quantified the QT adaptation lag in response to abrupt, step-like changes in HR induced by atrial pacing, in response to tilt test or during ambulatory recordings. Recent studies have introduced novel methods to quantify the QT adaptation lag to gradual, ramp-like HR changes in stress tests by evaluating the differences between the measured QT series and an estimated, memoryless QT series obtained from the instantaneous HR. These studies have observed the QT adaptation

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18

Mader, S. L., C. L. Downing, and E. Van Lunteren. "Effect of age and hypoxia on beta-adrenergic receptors in rat heart." Journal of Applied Physiology 71, no. 6 (1991): 2094–98. http://dx.doi.org/10.1152/jappl.1991.71.6.2094.

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Previous reports suggest that hypoxia downregulates cardiac beta-adrenergic receptors from young rats. Because aging alters response to stress, we hypothesized an age-related alteration in the response to hypoxia. Male Fischer-344 rats, aged 3 and 20 mo, were divided into control and hypoxic groups. The hypoxic rats were exposed to hypobaric hypoxia (0.5 atm) for 3 wk. After hypoxic exposure, body weight decreased, hematocrit increased, right ventricular weight increased, and left ventricular weight decreased in all animals. beta-Adrenergic receptor density declined after hypoxic exposure in t

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19

Colon-Echevarria, Claudia B., Tatiana Ortiz, Lizette Maldonado, et al. "Zoledronic Acid Abrogates Restraint Stress-Induced Macrophage Infiltration, PDGF-AA Expression, and Ovarian Cancer Growth." Cancers 12, no. 9 (2020): 2671. http://dx.doi.org/10.3390/cancers12092671.

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Multiple studies suggest that chronic stress accelerates the growth of existing tumors by activating the sympathetic nervous system. Data suggest that sustained adrenergic signaling can induce tumor growth, secretion of pro-inflammatory cytokines, and macrophage infiltration. Our goal was to study the role of adrenergic-stimulated macrophages in ovarian cancer biology. Cytokine arrays were used to assess the effect of adrenergic stimulation in pro-tumoral cytokine networks. An orthotopic model of ovarian cancer was used to assess the in vivo effect of daily restraint stress on tumor growth and

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20

Tomas, Megan. "Treatment of sleep disturbances in post-traumatic stress disorder." Mental Health Clinician 4, no. 2 (2014): 91–97. http://dx.doi.org/10.9740/mhc.n190104.

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Sleep disturbances are very common in patients suffering from post-traumatic stress disorder (PTSD) and can have various negative sequelae, including worsening of perceived levels of stress, depression, and suicidal ideation. Although PTSD treatment can lead to improved sleep in some patients, there are a number of patients whose sleep disturbances do not remit even after treatment and can persist long after the original trauma. There are various non-pharmacological and pharmacological treatment modalities that have been studied. Non-pharmacological therapies include image rehearsal therapy (I

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21

WONG, DONA L., T. C. TAI, DAVID C. WONG-FAULL, ROBERT CLAYCOMB, and RICHARD KVETNANSKY. "Genetic Mechanisms for Adrenergic Control during Stress." Annals of the New York Academy of Sciences 1018, no. 1 (2004): 387–97. http://dx.doi.org/10.1196/annals.1296.048.

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22

Rao, Fangwen, Lian Zhang, Jennifer Wessel, et al. "Adrenergic Polymorphism and the Human Stress Response." Annals of the New York Academy of Sciences 1148, no. 1 (2008): 282–96. http://dx.doi.org/10.1196/annals.1410.085.

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23

Montoya, P., Stuart Brody, Katja Beck, Ralf Veit, and Harald Rau. "Differential ?- and ?-adrenergic activation during psychological stress." European Journal of Applied Physiology 75, no. 3 (1997): 256–62. http://dx.doi.org/10.1007/s004210050157.

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24

Piquer, Beatriz, Diandra Olmos, Andrea Flores, et al. "Exposure of the Gestating Mother to Sympathetic Stress Modifies the Cardiovascular Function of the Progeny in Male Rats." International Journal of Environmental Research and Public Health 20, no. 5 (2023): 4285. http://dx.doi.org/10.3390/ijerph20054285.

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Background: Sympathetic stress stimulates norepinephrine (NE) release from sympathetic nerves. During pregnancy, it modifies the fetal environment, increases NE to the fetus through the placental NE transporter, and affects adult physiological functions. Gestating rats were exposed to stress, and then the heart function and sensitivity to in vivo adrenergic stimulation were studied in male progeny. Methods: Pregnant Sprague–Dawley rats were exposed to cold stress (4 °C/3 h/day); rats’ male progeny were euthanized at 20 and 60 days old, and their hearts were used to determine the β-adrenergic r

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25

Mohammadpour, Hemn. "Abstract P4-04-01: β2-adrenergic receptor signaling regulates metabolic pathways critical for the function of myeloid-derived suppressor cells". Cancer Research 82, № 4_Supplement (2022): P4–04–01—P4–04–01. http://dx.doi.org/10.1158/1538-7445.sabcs21-p4-04-01.

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Abstract Summary Nerve-driven chronic adrenergic stress can suppress anti-tumor immunity. However, details are still missing or poorly understood. Catecholamines (epinephrine, norepinephrine) released by sympathetic nerves can activate adrenergic receptors present on nearly every cell type including myeloid derived suppressor cells (MDSCs). MDSCs are increasingly recognized as critical players in tumor immunology because, in addition to their fundamental roles in suppressing effector NK cells, CD8+ T cells and CD4+ T cells, they also play a direct role in tumor growth, differentiation and meta

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26

Maryniak, Agnieszka, Andrzej Hasiec, Bartosz Duda, Michał Orczykowski, and Łukasz Szumowski. "Temperament, stress, and atrial fibrillation." Polish Psychological Bulletin 46, no. 2 (2015): 223–27. http://dx.doi.org/10.1515/ppb-2015-0030.

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Abstract In some patients with atrial fibrillation (AF), the causative agent of attack is stress (AF associated with adrenergic activity). In others, AF usually begins during relax or sleep (AF associated with vagal nerve dominance). This study aimed to investigate the individual factors associated with the adrenergic or vagal type of AF. This study included 138 patients with paroxysmal atrial fibrillation (AF). Sixty-eight patients reported that AF was frequently triggered by stress (sympathetic-type AF) and 70 patients reported that AF usually began during relaxation or sleep (vagal-type AF)

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27

Alexander, Jessica K., Ashleigh Hillier, Ryan M. Smith, Madalina E. Tivarus, and David Q. Beversdorf. "Beta-adrenergic Modulation of Cognitive Flexibility during Stress." Journal of Cognitive Neuroscience 19, no. 3 (2007): 468–78. http://dx.doi.org/10.1162/jocn.2007.19.3.468.

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Stress-induced activation of the locus ceruleus-norepinephrine (LC-NE) system produces significant cognitive and behavioral effects, including enhanced arousal and attention. Improvements in discrimination task performance and memory have been attributed to this stress response. In contrast, for other cognitive functions that require cognitive flexibility, increased activity of the LC-NE system may produce deleterious effects. The aim of the present study was to determine the effect of pharmacological modulation of the LC-NE system on stress-induced impairments in cognitive flexibility perform

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28

Suleymanoglu, Yilmaz, Dimitar Bakalov, Zafer Sabit, Vlayko Vodenicharov, Radka Tafradjiiska-Hadjiolova, and Hristina Nocheva. "The endogenous cannabinoid and the adrenergic systems in modulation of stress-response." Pharmacia 71 (January 17, 2024): 1–8. http://dx.doi.org/10.3897/pharmacia.71.e115659.

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In our modern, fast-paced society, excessive stress (or distress) is a major risk factor for developing a plethora of diseases. There are several neuromediatory systems in the brain that regulate the response to stress, including the adrenergic and endocannabinoid systems. In our experiments, we study the effects of the endocannabinoid system on the restrain stress-induced analgesia (r-SIA). The experiments were done on male Wistar rats. The animals were confined in special restrainers for a period of one hour. The animals were treated with Clonidine (at 4 mg/kg) – a prototypical α2-agonist; Y

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29

Arieli, Yehuda, Neomi Feinstein, Pnina Raber, Michal Horowitz, and Jacob Marder. "Heat stress induces ultrastructural changes in cutaneous capillary wall of heat-acclimated rock pigeon." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 4 (1999): R967—R974. http://dx.doi.org/10.1152/ajpregu.1999.277.4.r967.

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In heat-acclimated rock pigeons, cutaneous water evaporation is the major cooling mechanism when exposed at rest to an extremely hot environment of 50–60°C. This evaporative pathway is also activated in room temperature by a β-adrenergic antagonist (propranolol) or an α-adrenergic agonist (clonidine) and inhibited by a β-adrenergic agonist (isoproterenol). In contrast, neither heat exposure nor drug administration activates cutaneous evaporation in cold-acclimated pigeons. To elucidate the mechanisms underlying this phenomenon, we studied the role of the ultrastructure and permeability of the

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Reho, John J., and Steven A. Fisher. "The stress of maternal separation causes misprogramming in the postnatal maturation of rat resistance arteries." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 9 (2015): H1468—H1478. http://dx.doi.org/10.1152/ajpheart.00567.2015.

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We examined the effect of stress in the first 2 wk of life induced by brief periods of daily maternal separation on developmental programming of rat small resistance mesenteric arteries (MAs). In MAs of littermate controls, mRNAs encoding mediators of vasoconstriction, including the α1a-adrenergic receptor, smooth muscle myosin heavy chain, and CPI-17, the inhibitory subunit of myosin phosphatase, increased from after birth through sexual [postnatal day (PND) 35] and full maturity, up to ∼80-fold, as measured by quantitative PCR. This was commensurate with two- to fivefold increases in maximum

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Márquez-Ramírez, Cristian Adrián, Berenice Eridani Olmos-Orizaba, Claudia Isabel García-Berumen, et al. "Avocado Oil Prevents Kidney Injury and Normalizes Renal Vasodilation after Adrenergic Stimulation in Hypertensive Rats: Probable Role of Improvement in Mitochondrial Dysfunction and Oxidative Stress." Life 11, no. 11 (2021): 1122. http://dx.doi.org/10.3390/life11111122.

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Hypertension impairs the function of the kidney and its vasculature. Adrenergic activation is involved in these processes by promoting oxidative stress and mitochondrial dysfunction. Thus, the targeting of mitochondrial function and mitochondrial oxidative stress may be an approach to alleviate hypertensive kidney damage. Avocado oil, a source of oleic acid and antioxidants, improves mitochondrial dysfunction, decreases mitochondrial oxidative stress, and enhances vascular function in hypertensive rats. However, whether avocado oil improves the function of renal vasculature during the adrenerg

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Noyes, Russell. "Beta-Adrenergic Blocking Drugs in Anxiety and Stress." Psychiatric Clinics of North America 8, no. 1 (1985): 119–32. http://dx.doi.org/10.1016/s0193-953x(18)30713-5.

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Cristea, A. N. "Opioid and adrenergic types of behaviour to stress." European Neuropsychopharmacology 3, no. 3 (1993): 446–47. http://dx.doi.org/10.1016/0924-977x(93)90249-l.

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Jeong, Jae-Hoon, Hyun-Ji Park, Gyoo-Yong Chi, Yung-Hyun Choi, and Shin-Hyung Park. "An Ethanol Extract of Perilla frutescens Leaves Suppresses Adrenergic Agonist-Induced Metastatic Ability of Cancer Cells by Inhibiting Src-Mediated EMT." Molecules 28, no. 8 (2023): 3414. http://dx.doi.org/10.3390/molecules28083414.

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Previous studies have indicated that the adrenergic receptor signaling pathway plays a fundamental role in chronic stress-induced cancer metastasis. In this study, we investigated whether an ethanol extract of Perilla frutescens leaves (EPF) traditionally used to treat stress-related symptoms by moving Qi could regulate the adrenergic agonist-induced metastatic ability of cancer cells. Our results show that adrenergic agonists including norepinephrine (NE), epinephrine (E), and isoproterenol (ISO) increased migration and invasion of MDA-MB-231 human breast cancer cells and Hep3B human hepatoce

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Qiao, Guanxi, Minhui Chen, Hemn Mohammadpour, et al. "Adrenergic stress regulates the exhausted phenotype of T cells in the tumor microenvironment." Journal of Immunology 204, no. 1_Supplement (2020): 165.36. http://dx.doi.org/10.4049/jimmunol.204.supp.165.36.

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Abstract We have shown previously that host adrenergic stress (model of standard ambient temperature-induced chronic stress) slows tumor progression by enhancing CD8+ T-cell activation and limiting the suppressive function of myeloid-derived suppressor cells in the tumor microenvironment (TME). We also found that reducing/blocking β-adrenergic receptor (β-AR) signaling significantly improves anti-tumor immune responses and efficacy of immune checkpoint immunotherapy. It has been reported that expression of immune checkpoint receptors (e.g. PD-1, TIM3, LAG3) is characteristic of exhausted T-cel

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Donello, John E., Yun Guan, Mingting Tian, et al. "A Peripheral Adrenoceptor-mediated Sympathetic Mechanism Can Transform Stress-induced Analgesia into Hyperalgesia." Anesthesiology 114, no. 6 (2011): 1403–16. http://dx.doi.org/10.1097/aln.0b013e31821c3878.

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Background Stress has paradoxical effects on pain, causing stress-induced analgesia but also exacerbating pain via poorly understood mechanisms. Adrenergic neurotransmission is integral in pathways that regulate the response to both pain and stress. Hyperalgesia is often associated with enhanced adrenergic sensitivity of primary afferents, but sympathetic nervous system outflow has not been demonstrated to exacerbate pain perception after stress. Methods Rats or C57/BL6 wild-type mice treated with α-2 receptor antagonists or α-2A receptor knockout mice were exposed to ultrasonic noise stress o

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RAMRAKHIANI, S., A. SAFADI, J. FOLTZ, S. STRICKER, J. MAHENTHIRAN, and S. SAWADA. "Dopamine-atropine stress SPECT: An alternative adrenergic stress agent for Dobutamine SPECT." Journal of Nuclear Cardiology 12, no. 4 (2005): S115. http://dx.doi.org/10.1016/j.nuclcard.2005.06.050.

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Weeber, Peter, Stephanie Bremer, Jonas Haferanke, et al. "The Different Effects of Noradrenaline on Rhabdomyosarcoma and Ewing’s Sarcoma Cancer Hallmarks—Implications for Exercise Oncology." Onco 4, no. 4 (2024): 397–411. http://dx.doi.org/10.3390/onco4040028.

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Background: Exercise has beneficial effects on cancer and its treatment, but the underlying mechanisms are poorly understood. Some studies have linked the positive impact of exercise to catecholamine signaling. In contrast, cancer stress studies have typically reported that catecholamines worsen cancer hallmarks and outcomes. Here, we aimed to investigate whether adrenergic receptor isoform expression can explain the contradictory effects of catecholamines in cancer. Methods: We cultured two pediatric sarcoma cancer cell lines that either express (A673 cell line) or do not express (RD cell lin

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Prantil-Baun, Rachelle, William C. de Groat, Minoru Miyazato, Michael B. Chancellor, Naoki Yoshimura, and David A. Vorp. "Ex vivo biomechanical, functional, and immunohistochemical alterations of adrenergic responses in the female urethra in a rat model of birth trauma." American Journal of Physiology-Renal Physiology 299, no. 2 (2010): F316—F324. http://dx.doi.org/10.1152/ajprenal.00299.2009.

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Birth trauma and pelvic injury have been implicated in the etiology of stress urinary incontinence (SUI). This study aimed to assess changes in the biomechanical properties and adrenergic-evoked contractile responses of the rat urethra after simulated birth trauma induced by vaginal distension (VD). Urethras were isolated 4 days after VD and evaluated in our established ex vivo urethral testing system that utilized a laser micrometer to measure the urethral outer diameter at proximal, middle, and distal positions. Segments were precontracted with phenylephrine (PE) and then exposed to intralum

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Yates, Dustin T. "211 Overcoming the Growth Deficits Programmed by Maternofetal Stress." Journal of Animal Science 100, Supplement_3 (2022): 192. http://dx.doi.org/10.1093/jas/skac247.353.

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Abstract Prolonged maternofetal stress stunts placental development and causes fetal programming that reduces fetal growth and birthweight. Low birthweight due to intrauterine growth restriction (IUGR) of the fetus increases perinatal mortality. More commonly, however, it results in lifelong impairment of muscle growth capacity and metabolic function. In humans, low birthweight increases risk for obesity, diabetes, and other metabolic disorders by an estimated 18-fold. Similarly, low birthweight livestock exhibit greater early death loss, poor growth efficiency, and lower-quality carcasses at

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Werhahn, Stefanie Maria, Julia S. Kreusser, Marco Hagenmüller та ін. "Adaptive versus maladaptive cardiac remodelling in response to sustained β-adrenergic stimulation in a new ‘ISO on/off model’". PLOS ONE 16, № 6 (2021): e0248933. http://dx.doi.org/10.1371/journal.pone.0248933.

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On the one hand, sustained β-adrenergic stress is a hallmark of heart failure (HF) and exerts maladaptive cardiac remodelling. On the other hand, acute β-adrenergic stimulation maintains cardiac function under physiological stress. However, it is still incompletely understood to what extent the adaptive component of β-adrenergic signaling contributes to the maintenance of cardiac function during chronic β-adrenergic stress. We developed an experimental catecholamine-based protocol to distinguish adaptive from maladaptive effects. Mice were for 28 days infused with 30 mg/kg body weight/day isop

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Lechsner, Patrick, and Erika-Gyongyi Ban. "Alpha adrenergic receptors in clinical practice – Present and future." Acta Marisiensis - Seria Medica 68, no. 4 (2022): 145–49. http://dx.doi.org/10.2478/amma-2022-0030.

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Abstract In this review we discuss the adrenergic pathways for alpha 1 and alpha 2 receptors and the current as well as potential future medication targeting these receptors. Overall, there is ongoing research into a multitude of directions with a promising outlook for alpha 1 and alpha 2 adrenergic receptors. The alpha 1-adrenergic receptor subfamily is currently modulating only a modest number of nervous system functions due the fact, that only a relatively small number of selective commercial products are available. Chronic stress can affect the long-term depression of alpha 1 receptors. Re

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Yang, Shuo, Hong Ma, Liang Wang та ін. "The Role of β3-Adrenergic Receptors in Cold-Induced Beige Adipocyte Production in Pigs". Cells 13, № 8 (2024): 709. http://dx.doi.org/10.3390/cells13080709.

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After exposure to cold stress, animals enhance the production of beige adipocytes and expedite thermogenesis, leading to improved metabolic health. Although brown adipose tissue in rodents is primarily induced by β3-adrenergic receptor (ADRB3) stimulation, the activation of major β-adrenergic receptors (ADRBs) in pigs has been a topic of debate. To address this, we developed overexpression vectors for ADRB1, ADRB2, and ADRB3 and silenced the expression of these receptors to observe their effects on the adipogenic differentiation stages of porcine preadipocytes. Our investigation revealed that

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Longhurst, J. C., T. I. Musch, and G. A. Ordway. "O2 consumption during exercise in dogs--roles of splenic contraction and alpha-adrenergic vasoconstriction." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 3 (1986): H502—H509. http://dx.doi.org/10.1152/ajpheart.1986.251.3.h502.

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To examine the influence of alpha-adrenergic vasoconstriction on the aerobic capacity of dogs, we calculated O2 consumption (VO2) by the Fick method during submaximal and maximal exertion before and during alpha-adrenergic blockade with phentolamine. Regional blood flow was measured with radioactive microspheres. alpha-Adrenergic receptor blockade reduced VO2 by 12.9% during submaximal and 17.9% during maximal exercise. Arterial and venous lactic acid approximately doubled during both levels of stress in the presence of alpha-adrenergic receptor blockade. Calculated VO2 decreased because arter

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Barbiero, Silvia, Alberto Aimo, Vincenzo Castiglione, et al. "Healthy hearts at hectic pace: From daily life stress to abnormal cardiomyocyte function and arrhythmias." European Journal of Preventive Cardiology 25, no. 13 (2018): 1419–30. http://dx.doi.org/10.1177/2047487318790614.

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The hectic pace of contemporary life is a major source of acute and chronic stress, which may have a deleterious impact on body health . In the field of cardiovascular disease, acute emotional stress has been associated with coronary spasm and Takotsubo cardiomyopathy, whereas the manifestations of chronic stress have been overlooked, and most underlying pathophysiology remains to be elucidated. Chronic stress affects the neuronal circuitry composed of cortico-limbic structures and the nuclei regulating autonomic function, eliciting a sympatho-vagal imbalance, characterised by adrenergic activ

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Truijen, Jasper, Shyrin C. A. T. Davis, Wim J. Stok та ін. "Baroreflex sensitivity is higher during acute psychological stress in healthy subjects under β-adrenergic blockade". Clinical Science 120, № 4 (2010): 161–67. http://dx.doi.org/10.1042/cs20100137.

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Acute psychological stress challenges the cardiovascular system with an increase in BP (blood pressure), HR (heart rate) and reduced BRS (baroreflex sensitivity). β-adrenergic blockade enhances BRS during rest, but its effect on BRS during acute psychological stress is unknown. This study tested the hypothesis that BRS is higher during acute psychological stress in healthy subjects under β-adrenergic blockade. Twenty healthy novice male bungee jumpers were randomized and studied with (PROP, n=10) or without (CTRL, n=10) propranolol. BP and HR responses and BRS [cross-correlation time-domain (B

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Schmid, P. G., C. A. Whiteis, and D. D. Lund. "Ventricular hypertrophy and presynaptic regulation of sympathetic function." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (1990): H1375—H1381. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1375.

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In normal heart, presynaptic cholinergic muscarinic and alpha 2-adrenergic mechanisms contribute to regional variations in the rate constant of norepinephrine turnover (kNE), an index of sympathetic neural function. To evaluate these mechanisms in the hypertrophied heart, pulmonary artery-constricted and sham-operated guinea pigs were pretreated with 1) saline vehicle (control) or 2) a combination of quinuclidinyl benzilate (Q), a muscarinic cholinergic antagonist, and yohimbine (Y), an alpha 2-adrenergic antagonist. An increase in kNE was determined in multiple regions of heart from incorpora

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Pullinger, Gillian D., Sonya C. Carnell, Fathima F. Sharaff, et al. "Norepinephrine Augments Salmonella enterica-Induced Enteritis in a Manner Associated with Increased Net Replication but Independent of the Putative Adrenergic Sensor Kinases QseC and QseE." Infection and Immunity 78, no. 1 (2009): 372–80. http://dx.doi.org/10.1128/iai.01203-09.

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ABSTRACT Stress has long been correlated with susceptibility to microbial infection. One explanation for this phenomenon is the ability of pathogens to sense and respond to host stress-related catecholamines, such as norepinephrine (NE). In Gram-negative enteric pathogens, it has been proposed that NE may facilitate growth by mediating iron supply, or it may alter gene expression by activating adrenergic sensor kinases. The aim of this work was to investigate the relative importance of these processes in a model in which NE alters the outcome of Salmonella enterica serovar Typhimurium infectio

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Jackson, Benjamin T., George J. Piasecki, Herbert E. Cohn, and Wayne R. Cohen. "Control of fetal insulin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (2000): R2179—R2188. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2179.

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In this study, we investigated the way in which fetal insulin secretion is influenced by interrelated changes in blood glucose and sympathoadrenal activity. Experiments were conducted in late gestation sheep fetuses prepared with chronic peripheral and adrenal catheters. The fetus mounted a brisk insulin response to hyperglycemia but with only a minimal change in the glucose-to-insulin ratio, indicating a tight coupling between insulin secretion and plasma glucose. In well-oxygenated fetuses, α2-adrenergic blockade by idazoxan effected no change in fetal insulin concentration, indicating the a

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Martinez, Gilberto Gastelum, Marc E. Lippman, Barry Hudson, Philip Miller, Courtney Pine, and Yalini Anbalagan. "Abstract P1-04-19: Regulating Stress to Improve Antitumor Immunity in Breast Cancer Models." Clinical Cancer Research 31, no. 12_Supplement (2025): P1–04–19—P1–04–19. https://doi.org/10.1158/1557-3265.sabcs24-p1-04-19.

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Abstract Chronic stress significantly impacts cancer progression by fostering an immunosuppressive microenvironment that promotes tumor growth and diminishes therapeutic efficacy. Dysregulated stress hormones, like norepinephrine, mediate β-adrenergic stimulation, orchestrating a cascade of immunomodulatory events within the tumor microenvironment (TME). In estrogen receptor-positive (ER+) breast cancer, immunosuppression presents a challenge due to resistance to immunotherapy driven by molecular characteristics dampening antitumor immune responses. We explore the hypothesis that chronic stres

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