This study evaluates the reproducibility of individual differences in behaviorally evoked cardiovascular reactivity among 39 young adult males. Presented also are initial data describing idiosyncratic patterns of hemodynamic adjustment that may underlie pressor responses to laboratory stressors. Subjects were administered three experimental stressors (mental arithmetic, mirror tracing, and bicycle exercise) on two occasions, four weeks apart. Heart rate, blood pressure, and impedance-derived measurements of cardiac pre-ejection period, stroke index, cardiac index, and total peripheral resistance were obtained during baseline and task periods at each session. To index task-induced "reactivity," residualized (baseline-adjusted) change scores were calculated for all variables; percentage change from baseline was also calculated for impedance-derived hemodynamic measurements. Test-retest (inter-session) correlations were significant for nearly all baseline, task, and change-score measurements. The few exceptions included diastolic blood pressure changes during mirror tracing and bicycle exercise and changes in stroke index and peripheral resistance during mental arithmetic. Although virtually all baseline and task correlations exceeded .60, reactivity indices yielded consistently lower retest correlations (significant r's = .35-.78; median r = .49). In subsequent analyses, subsets of individuals were identified whose reactions to mental arithmetic at the first laboratory session reflected changes in either cardiac output (CI reactors, n = 9) or total peripheral resistance (TPR reactors, n = 6), or a combination of cardiac and vascular influences (Mixed reactors, n = 8). This typology of hemodynamic response: (a) was corroborated by corresponding group differences in heart rate, pre-ejection period, and stroke index; (b) was reproducible on retesting; and (c) showed some generalization to the mirror tracing task, though not to bicycle exercise.

To evaluate effects of acute mental stress on aspects of cellular immunity, lymphocyte populations and phytohemagglutinin (PHA)-stimulated T-cell mitogenesis were measured in 33 healthy young men, both before and immediately following subjects' performance of a frustrating, 21-minute laboratory task (Stroop test). Relative to baseline evaluations, post-task measurements showed a significant reduction in mitogenesis and alterations in various circulating lymphocyte populations; the latter included a diminished T-helper/T-suppressor cell ratio and an elevation in the number of natural killer cells. Eleven subjects assigned to a control (unstressed) condition exhibited no changes in lymphocyte populations, but did show an increase in T-cell proliferation, compared with pretask measurements.

To determine whether offspring of hypertensives show enhanced sympathetic nervous system activity, we evaluated several indices of sympathoadrenal activation and cardiovascular responsiveness to behavioral stimuli among 90 normotensive, young adult men having either one or two hypertensive parents (PH+(-), PH++) or normotensive parents only (PH--) (n = 30/group). Measurements included heart rate (HR) and blood pressure (BP) reactions to three mental stressors (the Stroop test, mental arithmetic, mirror tracing), a cold pressor test, postural adjustment (60 degrees upright tilt), isometric exercise and bicycle ergometry, as well as the 24-h excretion of catecholamines (epinephrine [E], norepinephrine [NE]) and venous plasma catecholamine concentrations, both at rest (seated and supine) and in response to the Stroop test and upright tilt. The three groups did not differ in age, education, body mass index (BMI), estimated aerobic fitness, resting HR, cardiac preejection period (PEP) and PEP:LVET (left ventricular ejection time) ratio, 24-h Na or K excretion, or fasting lipids, insulin or plasma renin activity. Resting systolic and diastolic BP varied as a function of parental hypertension, and were significantly higher in PH++ than among PH-- subjects (P < .05). No significant group difference was observed on any measure of plasma or urinary catecholamines, nor did offspring of hypertensives (PH++ or PH+-) showed greater HR or BP reactions than PH-- subjects to any of the several laboratory challenges. In sum, we find no evidence of enhanced sympathetic activity or heightened cardiovascular responsiveness among normotensive young adults who are familially predisposed to essential hypertension.

To evaluate the effects of mental stress on blood platelet activity, platelet secretion and aggregation were measured in 40 healthy young men, assigned in a 3:1 ratio to an experimental and control condition. After a baseline period, experimental subjects participated in a 21-minute, frustrating computer task (the Stroop test), while control subjects remained seated quietly for the same duration. Blood was drawn from all subjects immediately before and after the task period for assessment of platelet activity (secretion of ATP and aggregation in response to 5 and 20 microM ADP). Heart rate and blood pressure were also assessed at baseline and throughout the task period. Results indicated that measures of platelet secretion, heart rate, and blood pressure rose significantly from baseline to posttask assessments in subjects exposed to the experimental stressor (p < .05), but not among controls. These findings are consistent with the hypothesis that stress may potentiate coronary disease pathogenesis, in part, via activation of blood platelets and their associated effects on coronary artery occlusion and/or constriction.

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