Objective
Smokers often smoke during stressful events, which leads to large increases in cardiovascular measures such as blood pressure (BP) and heart rate (HR). Since 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, cross-over study in which BP, HR, plasma epinephrine, norepinephrine (NE) and cortisol concentrations were measured at rest, while smoking and during a speech and math task. Laboratory sessions occurred after one month of paroxetine and after one 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 values <0.001). After one month of paroxetine, NE and HR values were lower and cortisol values higher (vs. placebo) throughout the lab session (treatment effect p values < 0.001). Treatment × time effects were observed for blood pressure and heart rate (all p<0.01). For systolic and diastolic BP, a smaller increase (from baseline to measures during speech) was observed after paroxetine compared to placebo (both p <0.006). 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 (vs. 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.