title: Effect of paroxetine on physiological response to stress and smoking.
abstract: OBJECTIVE
  Smokers often smoke during stressful events, which leads to large increases in cardiovascular measures such as blood pressure (BP) and heart rate (HR). Because exaggerated cardiovascular response to stress is associated with cardiovascular disease risk, this study examined paroxetine's effect on the physiological response to combining stress and smoking.
  
  
  METHODS
  Sixty-two participants completed this randomized, double-blind, crossover study in which BP, HR, plasma epinephrine, norepinephrine, and cortisol concentrations were measured at rest, while smoking, and during a speech and math task. Laboratory sessions occurred after 1 month of paroxetine and after 1 month of placebo.
  
  
  RESULTS
  Significant increases occurred for all measures (except cortisol) during smoking, with further increases occurring during the speech task (time effect, p < .001). After 1 month of paroxetine, norepinephrine and HR values were lower and cortisol values were higher (versus placebo) throughout the laboratory session (treatment effect, p < .001). Treatment × time effects were observed for BP and HR (all, p < .01). For systolic and diastolic BP, a smaller increase (from baseline to measures during speech) was observed after paroxetine compared with placebo (both, p < .006). In both measures, the increase in response to smoking was similar for both treatments; however, the further increase during the speech was smaller when taking paroxetine (versus placebo).
  
  
  CONCLUSIONS
  This study suggests that paroxetine affects physiological response to stress in smokers. Further research is needed to determine the impact of these results on cardiovascular health. Trial Registration clinicaltrials.gov Identifier: NCT00218439.
authors.affiliation: Department of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN, USA. kotly001@umn.edu
authors.forename: Michael
authors.initials: M
authors.lastname: Kotlyar
authors.forename: Mustafa
authors.initials: M
authors.lastname: al'Absi
authors.forename: Paul
authors.initials: P
authors.lastname: Thuras
authors.forename: John P
authors.initials: JP
authors.lastname: Vuchetich
authors.forename: David E
authors.initials: DE
authors.lastname: Adson
authors.forename: April L
authors.initials: AL
authors.lastname: Nowack
authors.forename: Dorothy K
authors.initials: DK
authors.lastname: Hatsukami
mesh_terms: D000328:Adult; D018687:Antidepressive Agents, Second-Generation / Q000097:blood / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D018592:Cross-Over Studies; D004311:Double-Blind Method; D004837:Epinephrine / Q000097:blood; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D008297:Male; D009638:Norepinephrine / Q000097:blood; D017374:Paroxetine / Q000097:blood / Q000494:pharmacology*; D012907:Smoking / Q000097:blood / Q000503:physiopathology* / Q000523:psychology*; D013315:Stress, Psychological / Q000097:blood / Q000503:physiopathology* / Q000523:psychology*
chemical_list: D018687:Antidepressive Agents, Second-Generation; D017374:Paroxetine; D006854:Hydrocortisone; D009638:Norepinephrine; D004837:Epinephrine