1. Eleven untreated men with mild to moderate primary hypertension and 10 normotensive control subjects were studied at rest and during a mental stress test (Stroop colour word conflict test), which has previously been used in studies of hypertensive patients with regard to non-invasive cardiovascular variables and venous plasma catecholamine concentrations.
2. Heart rate, central cardiovascular pressures, cardiac output (thermodilution) and forearm blood flow (strain gauge plethysmography) were determined. Systemic and forearm vascular resistances were calculated. Arterial and venous plasma adrenaline and noradrenaline concentrations were measured by h.p.l.c., and arterial noradrenaline spillover and noradrenaline overflow from the forearm were assessed by isotope methodology ([3H]noradrenaline). Neuropeptide Y-like immunoreactivity was measured by radioimmunoassay.
3. In hypertensive patients heart rate, arterial blood pressure, cardiac output and forearm blood flow increased by 28%, 13%, 37% and 115%, respectively, and forearm and systemic vascular resistances decreased by 48% and 21%, respectively (P <0.001 for all responses), during stress. These responses were not different from those of the control group.
4. Arterial noradrenaline spillover rose by 63% and noradrenaline overflow from the forearm rose by 150% in the hypertensive patients in response to mental stress (P <0.001); no significant group differences could be demonstrated. However, the forearm noradrenaline overflow response to stress tended to be greater in the hypertensive group (P = 0.11). Arterial adrenaline concentrations doubled in both groups (P <0.001).
5. Arterial neuropeptide Y-like immunoreactivity increased slightly and similarly in the two groups (+7% in hypertensive patients and +9% in control subjects, P <0.05 for both) in response to mental stress. No net overflow of neuropeptide-Y-like immunoreactivity could be detected over the forearm.
6. It is concluded that the cardiovascular and sympatho-adrenal responses to mental stress evaluated in this study are similar in hypertensive patients and control subjects. Stress-induced vasodilatation occurs in the forearm despite signs of increased local sympathetic activity, indicating that powerful neurohormonal vasodilator mechanisms are activated by mental stress.