Terril L Verplaetse1, Philip H Smith2, Kathryn M Z Smith3, Lindsay M Oberleitner4, Sherry A McKee4. 1. Department of Psychiatry, Yale School of Medicine, 2 Church Street South, Suite 201, New Haven, CT, 06519, USA. terril.verplaetse@yale.edu. 2. Department of Community Health and Social Medicine, CUNY School of Medicine, New York, NY, USA. 3. Division on Substance Abuse, Department of Psychiatry, Columbia University Medical Center/New York State Psychiatric Institute, New York, NY, USA. 4. Department of Psychiatry, Yale School of Medicine, 2 Church Street South, Suite 201, New Haven, CT, 06519, USA.
Abstract
BACKGROUND: We had previously demonstrated that guanfacine, an α2a-adrenergic agonist, attenuated the effect of stress on smoking-lapse behavior in regular daily smokers. Heart rate variability (HRV), a measure of vagal activity, may be a potential mechanism underlying the relationship between stress, smoking, and relapse. METHODS: We examined whether guanfacine (0 mg/day vs. 3 mg/day; n = 26) altered changes in high-frequency heart rate variability (HF-HRV) following stress and ad-lib smoking using a validated laboratory analogue of smoking-lapse behavior. All participants completed a parent study evaluating the effects of guanfacine on stress-precipitated smoking. Each subject completed two laboratory sessions assessing the effects of guanfacine on HF-HRV following stress imagery (vs. neutral imagery; order counterbalanced) and smoking. RESULTS: Results demonstrated that guanfacine did not increase tonic levels of HF-HRV relative to placebo. Following the stress versus neutral imagery manipulation (prior to ad-lib smoking), there were no significant changes in HF-HRV in the placebo group. In contrast, guanfacine increased phasic HF-HRV following stress imagery and decreased HF-HRV following neutral imagery. Ad libitum smoking following both the stress and neutral conditions decreased HF-HRV in the placebo group across both imagery conditions. In contrast, guanfacine attenuated stress- and smoking-related decreases in phasic HF-HRV relative to the neutral imagery condition. CONCLUSIONS: This is the first demonstration that a noradrenergic target altered dynamic changes in HF-HRV in response to stress and smoking, suggesting that guanfacine alters HF-HRV response to stress. Findings support current theories which suggest that phasic changes in HRV are an important marker of the stress response.
RCT Entities:
BACKGROUND: We had previously demonstrated that guanfacine, an α2a-adrenergic agonist, attenuated the effect of stress on smoking-lapse behavior in regular daily smokers. Heart rate variability (HRV), a measure of vagal activity, may be a potential mechanism underlying the relationship between stress, smoking, and relapse. METHODS: We examined whether guanfacine (0 mg/day vs. 3 mg/day; n = 26) altered changes in high-frequency heart rate variability (HF-HRV) following stress and ad-lib smoking using a validated laboratory analogue of smoking-lapse behavior. All participants completed a parent study evaluating the effects of guanfacine on stress-precipitated smoking. Each subject completed two laboratory sessions assessing the effects of guanfacine on HF-HRV following stress imagery (vs. neutral imagery; order counterbalanced) and smoking. RESULTS: Results demonstrated that guanfacine did not increase tonic levels of HF-HRV relative to placebo. Following the stress versus neutral imagery manipulation (prior to ad-lib smoking), there were no significant changes in HF-HRV in the placebo group. In contrast, guanfacine increased phasic HF-HRV following stress imagery and decreased HF-HRV following neutral imagery. Ad libitum smoking following both the stress and neutral conditions decreased HF-HRV in the placebo group across both imagery conditions. In contrast, guanfacine attenuated stress- and smoking-related decreases in phasic HF-HRV relative to the neutral imagery condition. CONCLUSIONS: This is the first demonstration that a noradrenergic target altered dynamic changes in HF-HRV in response to stress and smoking, suggesting that guanfacine alters HF-HRV response to stress. Findings support current theories which suggest that phasic changes in HRV are an important marker of the stress response.
Authors: L Bernardi; J Wdowczyk-Szulc; C Valenti; S Castoldi; C Passino; G Spadacini; P Sleight Journal: J Am Coll Cardiol Date: 2000-05 Impact factor: 24.094
Authors: Douglas E Jorenby; J Taylor Hays; Nancy A Rigotti; Salomon Azoulay; Eric J Watsky; Kathryn E Williams; Clare B Billing; Jason Gong; Karen R Reeves Journal: JAMA Date: 2006-07-05 Impact factor: 56.272
Authors: M Pagani; G Mazzuero; A Ferrari; D Liberati; S Cerutti; D Vaitl; L Tavazzi; A Malliani Journal: Circulation Date: 1991-04 Impact factor: 29.690
Authors: V K Yeragani; R Pohl; R Berger; R Balon; C Ramesh; D Glitz; K Srinivasan; P Weinberg Journal: Psychiatry Res Date: 1993-01 Impact factor: 3.222