1. Twenty-five normotensive men were subjected to two periods of mental stress involving a cognitive task and a competitive electronic game. Plasma catecholamines, heart rate and blood pressure were measured before and during mental stress. Responsiveness to β-adrenoceptor stimulation was also determined in each subject by measurement of heart rate responses to bolus injections of isoprenaline.

2. Both periods of mental stress were associated with significant increases in systolic and diastolic blood pressures, heart rate and plasma adrenaline, but not plasma noradrenaline. Heart rate responses to mental stress varied widely, with increases ranging from 1 to 48 (mean ± sd 13.5 ± 10.6) beats/min for the cognitive task and from 2 to 49 (20.4 ± 14.0) beats/min for the electronic game. Systolic blood pressure responses also varied widely and showed significant positive correlations with heart rate responses.

3. Significant relationships were found between heart rate responses to both forms of mental stress and cardiac sensitivity to isoprenaline, subjects with low responsiveness to β-adrenoceptor stimulation tending to have smaller heart rate responses to mental stress than subjects with high responsiveness to β-adrenoceptor stimulation. Relationships were also found between plasma adrenaline responses and heart rate responses to mental stress, although these did not reach significance. Considerably improved relationships were found when heart rate responses were correlated with a single variable generated from the product of the adrenaline response and the inverse of the dose of isoprenaline required to raise heart rate by 25 beats/min.

4. It is concluded that wide variation is shown between different individuals in responsiveness to β-adrenoceptor stimulation and that this is an important factor in the variability between individuals in heart rate and systolic blood pressure responses to mental stress. Both catecholamines and adrenoceptor-mediated responses to catecholamines should be examined when determining the physiological basis for differences in cardiovascular reactivity to mental stress between individuals or groups.

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