2005
DOI: 10.1161/01.hyp.0000153517.44295.07
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Sleep Deprivation Potentiates Activation of Cardiovascular and Catecholamine Responses in Abstinent Alcoholics

Abstract: Abstract-Alcohol dependence is associated with an increased incidence of hypertension and cardiac arrhythmias, but the triggering mechanisms are not known. Sleep loss, common in alcohol-dependent patients, causes an activation of the sympathetic nervous system. To determine whether sleep deprivation induces differential cardiovascular and sympathetic responses in alcohol dependence, we measured heart rate, blood pressure, and circulating sympathetic catecholamines in 36 abstinent alcohol-dependent men and 36 a… Show more

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Cited by 50 publications
(35 citation statements)
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“…Among patients with insomnia, increase in norepinephrine, epinephrine, and other markers of sympathetic outflow (as measured by blood pressure, heart rate variability, and impedance cardiography) occurs (Bonnet and Arand, 1997;Lanfranchi et al, 2009;Riemann, 2010;De Zambotti et al, 2011;Vgontzas and Fernandez-Mendoza et al, 2013). Further, it appears that sleep disturbance causes such sympathetic activation, as experimental sleep deprivation induces a similar increase in markers of sympathetic activity (Irwin and Thompson et al, 1999;Irwin and Ziegler, 2005). Interestingly, increase in urinary catecholamine and levels of their metabolites are more likely to occur in those insomnia patients who also report short sleep duration, a pattern similar to the greater activation of inflammatory biomarkers in this more severe phenotype (Vgontzas et al, 2013).…”
Section: Sympathetic Nervous Systemmentioning
confidence: 99%
“…Among patients with insomnia, increase in norepinephrine, epinephrine, and other markers of sympathetic outflow (as measured by blood pressure, heart rate variability, and impedance cardiography) occurs (Bonnet and Arand, 1997;Lanfranchi et al, 2009;Riemann, 2010;De Zambotti et al, 2011;Vgontzas and Fernandez-Mendoza et al, 2013). Further, it appears that sleep disturbance causes such sympathetic activation, as experimental sleep deprivation induces a similar increase in markers of sympathetic activity (Irwin and Thompson et al, 1999;Irwin and Ziegler, 2005). Interestingly, increase in urinary catecholamine and levels of their metabolites are more likely to occur in those insomnia patients who also report short sleep duration, a pattern similar to the greater activation of inflammatory biomarkers in this more severe phenotype (Vgontzas et al, 2013).…”
Section: Sympathetic Nervous Systemmentioning
confidence: 99%
“…The proinflammatory effects of sleep restriction may, at least partly, be mediated by stress activation, i.e. sympathetic and/or cortisol activation [41][42][43]. In addition, the group of KNUTSON and VAN CAUTER [44] speculated that the adverse impact of sleep deprivation on appetite regulation is likely to be driven by increased activity in neuronal populations expressing the excitatory peptides orexins, which promote both waking and feeding [44][45][46].…”
Section: Physiological and Clinical Datamentioning
confidence: 99%
“…The health of the individual may also interact with sleep deprivation to affect SNS functions. For example, a partial night of sleep deprivation induces a greater increase in heart rate and circulating NE and EPI concentrations in men with alcohol dependence compared to controls [146] , an effect that is sustained after nights of partial and recovery sleep.…”
Section: Sleep Deprivation and Catecholaminesmentioning
confidence: 99%