Lynn A. Durel’s research while affiliated with University of Miami and other places

This study addresses the hypothesis that electrocardiographic T-wave amplitude is influenced by beta-adrenergic stimulation of the heart. Beta-adrenergic activity was manipulated both pharmacologically and through behavioral challenge. Under resting conditions, 12 healthy men underwent infusion of placebo and then the beta-agonist, isoproterenol, and the beta-blocker, propranolol, in a counterbalanced, crossover design. During infusion of placebo, subjects also underwent two behavioral challenges, a structured interview and mental arithmetic. Analysis of the resting data indicated that propranolol produced a significant increase in T-wave amplitude, and isoproterenol produced significant T-wave amplitude attenuation. As previously reported, drug effects were also in evidence for heart rate. Behaviorally-induced reduction of T-wave amplitude was observed for mental arithmetic but not structured interview, which again paralleled heart rate data. Both pharmacological and behavioral data reported in this study support the hypothesis that the T-wave is significantly affected by beta-sympathetic influence on the heart. However, a nonspecific effect of heart rate change on T-wave amplitude would also account for these results. The findings are discussed in terms of their implications for the utility of T-wave amplitude in psychophysiological research.

This study compared the effects of beta-blockers differing in degree of central nervous system penetration on Type A behavior and cardiovascular reactivity to mental stress. Forty-six male hypertensives were assigned randomly to receive either highly lipophilic and nonselective propranolol, hydrophilic and cardioselective atenolol, the diuretic hydrochlorothiazide, or placebo. Subjects were administered parallel forms of the Structured Interview (SI) and performed mental arithmetic and a cognitive task prior to and after 6 weeks of therapy. Results indicated that diuretic and placebo subjects (subsequently combined into a single control group) did not differ and that both beta-blockers reduced heart rate but not blood pressure reactivity to mental stress (p less than 0.02), an effect that was strongest during the mental arithmetic test. Analysis of SI components indicated a reduction only in explosive speech for beta-blockers versus controls (p less than 0.05). For global SI classifications, seven out of 12 subjects (58%) receiving propranolol, three of 12 (25%) receiving atenolol, and four of 22 control subjects (18%) became less Type A (p less than 0.05). These data do not replicate results of a prior study obtained with atenolol and suggest that only a subset of hypertensive individuals show reduced Type A behavior with propranolol. Central nervous system mechanisms may be important in producing these effects.

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.

Clinically effective anxiolytic drugs generally increase responding that is suppressed by punishment. Although beta-adrenergic antagonists have been reported to reduce anxiety in humans, such effects have not been reported reliably in animal punishment procedures. In the present study, three pigeons were trained to key peck under a multiple schedule. In the presence of a white light every thirtieth response produced grain. In the presence of a red light every thirtieth response produced grain and electric shock which suppressed responding to approximately 10 percent of that occurring in the alternate component. Propranolol (1.0-5.6 mg/kg) and, less reliably, atenolol significantly increased punished responding in a dose-related manner; propranolol effects were approximately twice as large as those of atenolol. Both drugs no more than weakly increased unpunished response rates at doses that increased punished responding. These results suggest that beta-blockers have an antianxiety effect on punished behavior, and that peripheral beta-blockade, the predominant action of beta-blockers regardless of whether they readily penetrate the brain, is likely to be involved in this effect.

Beta-adrenergic blocking drugs have a variety of psychologic and behavioral effects. Among those effects considered beneficial, decreases in anxiety and type A behavior and improved psychologic reactions to acutely stressful situations have been observed. The somatic manifestations of these conditions appear to be reduced more effectively by beta blockade than are cognitive or attitudinal manifestations. Because of this, the emotion- related influences of these drugs are primarily thought to reflect the inhibition of peripheral beta-adrenergic responses. This article reviews evidence for these effects and describes cautions regarding unwanted psychologic and behavioral side effects of beta blockers with different pharmacologic properties. For cardiac patients disturbed, by somatic symptoms, beta blockers may provide a means for reducing psychobiologic effects of stress, with relatively little impact on task performance.

Argues that Type A (coronary prone) behavior may reflect excessive sympathetic responsiveness to environmental stressors rather than just person–situation interactions, and that an underlying biological or psychobiological factor might affect the expression of Type A behavior. Data consistent with a psychobiological view are provided by studies of (1) patients undergoing coronary bypass surgery and (2) the effects of beta-adrenergic blocking drugs in decreasing Type A behavior. A somatopsychic model of Type A behavior is formulated that considers the role of sympathetic nervous system responses and the processing of information about these responses in contributing to emotional behavior. (PsycINFO Database Record (c) 2012 APA, all rights reserved)

The present correlational study compared behavioral and psychophysiological characteristics of coronary patients who were either medicated or not medicated with the beta-adrenergic blocking drug propranolol. Eighty-eight patients were given a structured Type A interview (SI) and a history quiz while heart rate and blood pressure were monitored. Data were analyzed controlling for age, sex, extent of coronary artery disease, and history of angina. Results indicated that patients taking propranolol (n = 65) were significantly lower in intensity of Type A behavior than patients not taking propranolol (n = 23). No effects were obtained for patients medicated or not medicated with diuretics, nitrates, or other CNS active drugs. Propranolol patients also showed lesser heart rate and rate-pressure product responses to the interview, but did not differ in blood pressure responses. Components of Type A which were lower in propranolol patients included speech stylistics (loud/explosive, rapid/accelerated, potential for hostility). Content of responses to the SI and scores on the Jenkins Activity Survey did not differ between the groups. An explanation for these results is offered in terms of the effects of propranolol on peripheral sympathetic responses, and evidence for a physiological substrate for Type A behavior. A conceptualization of the Type A pattern in terms of cognitive and physiological components is advanced, and implications for clinical intervention are discussed.