The purpose of the present study was to determine how cigarette smoking and psychological stress combine to affect cardiovascular function. Stress was operationally defined as playing a series of difficult video games under challenging instructional conditions. Following an initial test game, 51 smokers were randomly assigned to a 2 (smoke vs. sham smoke) X 2 (stress vs. no stress) design. The results showed that the subjects who sham smoked (inhaled unlit cigarettes) under no stress evidenced minimal changes in cardiovascular parameters. Subjects who smoked under no stress evidenced approximately 12 mmHg increase in systolic blood pressure (SBP) and 9 mmHg increases in diastolic blood pressure (DBP), and a 15 beat-per-minute increase in heart rate (HR). These effects were similar in magnitude to those seen in subjects who sham smoked under stress. By contrast, subjects who smoked under stress showed markedly larger increases in all cardiovascular parameters, approximately doubling the magnitude of the observed response over that seen with either smoking or stress alone. Correlational analyses suggested the presence of stable individual differences in autonomic lability or sensitivity. Possible mechanisms are suggested whereby stress and smoking may combine to heighten the risk for coronary disease.

The present study examined the acute effects of drugs that stimulate or block sympathetic nervous system activity on components of Type A behavior, affect, and cardiovascular responses to mental stressors. Either propranolol (a beta-adrenergic blocker), isoproterenol (a beta-agonist), or placebo was infused intravenously at different times in 12 healthy males. In two sessions, placebo (saline) was administered first, followed by a structured interview, challenging mental arithmetic test, and completion of affect scales. The procedure was then repeated with one of the active drugs, presented in counterbalanced order. Results indicated reliable drug effects on both heart rate (HR) and systolic blood pressure (SBP) reactivity to the tasks, with change scores to the tasks markedly increased by isoproterenol. Anxiety and hostility ratings paralleled results for HR and BP, with much of this effect being due to higher affect ratings for isoproterenol. The effect of the drugs on Type A behavior was unexpected, with global Type A and several components lowered by isoproterenol and unaffected by propranolol. These data are discussed in terms of the interfering effects of anxiety on Type A speech components. The influence of isoproterenol on affect and reactivity might reflect the physiologic action of a beta 2-adrenergic positive feedback loop which increases release of endogenous norepinephrine, and/or potentiating effects of emotion on reactivity to stress.

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