Cardiovascular and sympatho-adrenal responses to mental stress with special reference to the regulation of human forearm blood flow

Abstract

The cardiovascular and sympatho-adrenal responses to a standardized mental stress test (Stroop's colour word conflict test CWT) were studied in 63 healthy and 11 hypertensive men by intraarterial pressure measurements, forearm blood flow by occlusion plethysmography and noradrenaline (NA) and adrenaline (ADR) determinations in arterial and venous plasma. One study included central hemodynamics by right heart catheterization and NA turnover by an isotope dilution method, permitting studies of NA kinetics in the whole body and in a regional vascular bed (the forearm) in hypertensive patients and age-matched controls.

CWT elicited marked hemodynamic changes in healthy subjects. There were increases in heart rate (+17 beats per minute), cardiac output (+46%), systolic (+18%) and diastolic (+19%) arterial brachial pressures and forearm blood flow (+140%) and decreases in systemic (-21%) and forearm (-44%) vascular resistances. There was a transient increase (+14%) in pulmonary arterial pressure. Arterial and venous plasma NA increased by about 40%, total body NA spillover by 73% and forearm NA overflow by about 100%. Arterial ADR increased by 147%. Stress responses in the hypertensive patients were essentially the same as in the control group.

The effects of calcium channel blockade on hemodynamics and catecholamines at rest and during CWT were evaluated in 11 hypertensives and in 10 controls. Intravenous felodipine lowered arterial pressure by decreasing systemic vascular resistance. Heart rate and cardiac output were increased, as were arterial NA spillover and forearm NA overflow. During long term treatment in X hypertensives, there was a further decrease in arterial pressure, due to the return of heart rate and cardiac output to baseline and preserved low systemic vascular resistance. However, arterial NA spillover and forearm NA overflow remained elevated. Hemodynamic and sympatho-adrenal stress-responses were essentially preserved during both acute and long term treatment. There were no main differences in stress reactivity between hypertensives and controls during acute calcium channel blockade.

Mechanisms contributing to the sustained forearm vasodilator response to CWT were systematically evaluated by different interventions in healthy subjects performing CWT. Venous plasma ADR concentrations were compared at similar decreases in forearm vascular resistances during intraarterial ADR, intravenous ADR and CWT, respectively, in 11 subjects. The average contribution of ADR to stress-induced forearm vasodilation was calculated to be about 30%. In concert with these results, regional beta-blockade in 18 subjects by intraarterial propranolol during CWT clearly attenuated the forearm vasodilator response. Forearm vasodilation in response to CWT was fully preserved after axillary blockade in 12 subjects; thus, stress responses were independent of nerve activity in the forearm vascular bed. Accordingly, regional cholinergic blockade in 18 subjects by intraarterial atropine during CWT elicited no clear-cut changes in forearm vascular resistance.

The dependence of forearm NA overflow on regional blood flow was evaluated in 7 healthy subjects. Forearm NA overflow was compared during CWT and regional vasodilation without sympathetic activation, i. e. intra-arterial infusion of sodium nitroprusside. In most subjects, forearm NA overflow increased more during mental stress than during nonspecific vasodilation, but the flow dependence of NA overflow was considerable.

In conclusion, a standardized mental stress test elicited marked hemodynamic responses and increased total and regional forearm sympathetic activity in healthy individuals. Stress responses were similar in a group of patients with mild to moderate hypertension. Stress reactivity was not altered by acute calcium channel blockade (felodipine) in either hypertensives or controls. During long term treatment of hypertensives with felodipine, heart rate returned towards baseline values, but total and regional forearm sympathetic activity remained elevated. The marked forearm vasodilation during mental stress was not caused by decreased sympathetic activity, nor was it an effect of active cholinergic vasodilation or other neurogenic mechanisms. The vasodilation was partly mediated by circulating ADR and beta-adrenoceptor stimulation, but a main explanatory factor is still lacking. Forearm NA overflow, as assessed by an isotope dilution method, may be a useful marker of regional sympathetic nerve activity, but is considerably influenced by increases in regional blood flow.