Effects of beta-adrenergic blockade on immunologic and cardiovascular changes induced by mental stress.

Benschop, Robert J.; Nieuwenhuis, E. E. S.; Tromp, Erna; Godaert, G. L. R.; Ballieux, R. E.; Doornen, Lorenz J.P. van

doi:10.1161/01.cir.89.2.762

Cited by 165 publications

(72 citation statements)

References 39 publications

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“…Direct effects of sympathetic activity on the function, number, and subset distribution of circulating lymphocytes have been described. 23,24 All of these mechanisms may have contributed to the observed associations. However, our measures of age, insulin, smoking, hypertension, physical activity, atherosclerosis, diabetes, and cancer did not explain these relationships.…”

Section: Mechanismsmentioning

confidence: 98%

Low Heart Rate Variability in a 2-Minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes

et al. 2000

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Background-Low heart rate variability (HRV) is associated with a higher risk of death in patients with heart disease and in elderly subjects and with a higher incidence of coronary heart disease (CHD) in the general population. Methods and Results-We studied the predictive value of HRV for CHD and death from several causes in a population study of 14 672 men and women without CHD, aged 45 to 65, by using the case-cohort design. At baseline, in 1987 to 1989, 2-minute rhythm strips were recorded. Time-domain measures of HRV were determined in a random sample of 900 subjects, for all subjects with incident CHD (395 subjects), and for all deaths (443 subjects) that occurred through 1993. Relative rates of incident CHD and cause-specific death in tertiles of HRV were computed with Poisson regression for the case-cohort design. Subjects with low HRV had an adverse cardiovascular risk profile and an elevated risk of incident CHD and death. The increased risk of death could not be attributed to a specific cause and could not be explained by other risk factors. Conclusions-Low HRV was associated with increased risk of CHD and death from several causes. It is hypothesized that low HRV is a marker of less favorable health.

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Section: Mechanismsmentioning

confidence: 98%

Low Heart Rate Variability in a 2-Minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes

et al. 2000

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“…Administration of epinephrine and norepinephrine in vivo transiently increases circulating T lymphocyte numbers (9,14). Furthermore, treatment with ␤-adrenoceptor antagonists inhibits the increase in circulating lymphocytes induced by exercise or psychological (4,29). In a rat study, low-dose epinephrine administration significantly enhanced skin DTH response and produced a significant increase in the number of T lymphocytes in the lymph nodes draining the site of DTH reaction (13).…”

Section: ϫ8mentioning

confidence: 99%

Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress

Okutsu¹,

Ishii²,

Niu³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The aim of this study was to elucidate the mechanism responsible for lymphopenia after exercise. Seven young healthy men volunteered for this study. Peripheral blood mononuclear cells (PBMC) were cultured with cortisol and analyzed for C-X-C motif chemokine receptor 4 (CXCR4) expression by flow cytometry. To determine the effects of exercise, subjects performed exhaustive cycling exercise. PBMC were cultured with plasma obtained before and after the cycling exercise. Alternatively, PBMC obtained before and after exercise were cultured without plasma or glucocorticoid to examine whether PBMC were primed in vivo for CXCR4 expression. We analyzed cortisol-or plasma-treated PBMC to determine their ability to migrate through membrane filters in response to stromal cell-derived factor 1␣/CXCL12. Cortisol doseand time-dependently augmented CXCR4 expression on T lymphocytes, with Ͻ6 h of treatment sufficient to augment CXCR4 on T lymphocytes. Postexercise plasma also augmented CXCR4 expression. Cortisol or postexercise plasma treatment markedly enhanced migration of T lymphocytes toward CXCL12. Augmentation of CXCR4 on T lymphocytes by cortisol or plasma was effectively blocked by the glucocorticoid receptor antagonist RU-486. Thus exercise-elicited endogenous cortisol effectively augments CXCR4 expression on T lymphocytes, which may account for lymphopenia after exercise. chemokine receptor; glucocorticoid; T cell distribution

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“…Most laboratory studies in psychoneuroimmunology make use of stressors that require mental effort and that are characterized by their potential to evoke a classic fight-flight cardiovascular response pattern (eg, mental arithmetic, Stroop task, and reaction tasks) (77)(78)(79)(80)(81)(82)(83)(84). This clearly being the dominant paradigm, it may become overlooked that there is a body of literature showing that many stressful situations do not necessarily elicit a substantial cardiovascular response and may even be associated with a reduced HR (85)(86)(87)(88)(89).…”

Section: J a Bosch Et Almentioning

confidence: 99%

Salivary MUC5B-Mediated Adherence (Ex Vivo) of Helicobacter pylori During Acute Stress

Bosch

Geus

Ligtenberg

et al. 2000

Psychosomatic Medicine

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Objective: Biochemical host defenses at mucosal sites, such as the oral cavity, play a key role in the regulation of microbial ecology and the prevention of infectious disease. These biochemical factors have distinct features, some of which benefit the host and some that benefit bacteria. We investigated the effects of acute stress on the salivary levels of the carbohydrate structure sulfo-Lewis a (sulfo-Le a ), which is linked to the mucosal glycoprotein MUC5B. Sulfo-Le a was recently identified as an adhesion molecule for Helicobacter pylori; therefore, we also measured saliva-mediated adherence (ex vivo) of H. pylori. The oral cavity is suspected to be involved in the transmission of H. pylori. Methods: Saliva was collected from 17 undergraduates before (baseline), during (stress), and after (recovery) exposure to a video showing surgical procedures. In addition, blood pressure, an impedance cardiogram, and an electrocardiogram were recorded. Results: During stressor exposure, participants reported increased state anxiety. In addition, stroke volume increased and heart rate decreased. The stressor induced a strong increase in salivary sulfo-Le a concentration (U/ml), sulfo-Le a output (U/min), sulfo-Le a /total protein ratio (U/mg protein), and saliva-mediated adherence (ex vivo) of H. pylori. As expected, sulfo-Le a concentration correlated with the adherence of H. pylori (r ϭ 0.72, p Ͻ .05). It was demonstrated that the observed adherence was induced by MUC5B and that the carbohydrate structure sulfo-Le a contributed to this process. Conclusions: Our study demonstrated a direct link between stress-mediated biochemical changes and altered host-microbe interactions in humans. Increased bacterial adherence may be a contributing factor in the observed relationship between stress and susceptibility to infectious disease.

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Effects of beta-adrenergic blockade on immunologic and cardiovascular changes induced by mental stress.

Cited by 165 publications

References 39 publications

Low Heart Rate Variability in a 2-Minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes

Low Heart Rate Variability in a 2-Minute Rhythm Strip Predicts Risk of Coronary Heart Disease and Mortality From Several Causes

Cortisol-induced CXCR4 augmentation mobilizes T lymphocytes after acute physical stress

Salivary MUC5B-Mediated Adherence (Ex Vivo) of Helicobacter pylori During Acute Stress

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