1. Eleven untreated men with mild to moderate primary hypertension and
10 normotensive control subjects were studied at rest and during a me
ntal stress test (Stroop colour word conflict test), which has previou
sly been used in studies of hypertensive patients with regard to non-i
nvasive cardiovascular variables and venous plasma catecholamine conce
ntrations. 2. Heart rate, central cardiovascular pressures, cardiac ou
tput (thermodilution) and forearm blood flow (strain gauge plethysmogr
aphy) were determined. Systemic and forearm vascular resistances were
calculated. Arterial and venous plasma adrenaline and noradrenaline co
ncentrations were measured by h.p.l.c., and arterial noradrenaline spi
llover and noradrenaline overflow from the forearm were assessed by is
otope methodology ([H-3]noradrenaline). Neuropeptide Y-like immunoreac
tivity was measured by radioimmunoassay. 3. In hypertensive patients h
eart rate, arterial blood pressure, cardiac output and forearm blood f
low 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 d
ifferent from those of the control group. 4. Arterial noradrenaline sp
illover rose by 63% and noradrenaline overflow from the forearm rose b
y 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 gr
eater in the hypertensive group (P=0.11). Arterial adrenaline concentr
ations doubled in both groups (P< 0.001). 5. Arterial neuropeptide Y-l
ike immunoreactivity increased slightly and similarly in the two group
s (+7% in hypertensive patients and +9% in control subjects, P<0.05 fo
r both) in response to mental stress. No net overflow of neuropeptide-
Y-like immunoreactivity could be detected over the forearm. 6. It is c
oncluded that the cardiovascular and sympatho-adrenal responses to men
tal stress evaluated in this study are similar in hypertensive patient
s and control subjects. Stress-induced vasodilatation occurs in the fo
rearm despite signs of increased local sympathetic activity, indicatin
g that powerful neurohormonal vasodilator mechanisms are activated by
mental stress.