CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 1, February 2012
32
AFRICA
result of receptor down-regulation and, therefore, an experienc-
ing of chronic stress and/or emotional exhaustion is revealed.
29
Results of urine analyses for cortisol, collected over eight to
24 hours and indicating chronic stress
6
are, however, not avail-
able yet and this is a limitation of this sub-study. Resting cortisol
values in both men and women were significantly lower during
sampling time 2 compared to sampling time 1. Our data confirm
the circadian rhythm that cortisol follows on the observed corti-
sol concentration at certain times during the day.
31
Both hypertensive men and women demonstrated higher
levels of stress, as indicated by high-normal resting cortisol and
glucose values, as well as increased vascular responsiveness
during mental stress in cortisol sampling time 1. It was also
apparent that in men and women, independent of blood pressure
status, their high-normal blood glucose levels, which were above
4.9 mmol/l, could imply increased cardiovascular risk.
32
In developing countries where cultural disruptions are appar-
ent, such as experienced by black South Africans, this could
increase stress and therefore accentuate their CVD risk. This
could especially hold true in black Africans with an inherent
predisposition to increased salt sensitivity and sympathetic
nervous system hyperactivity.
11,26
Findings from other studies
29,33
indicated a synergistic effect of vascular mechanisms and norepi-
nephrine on cortisol, which may further impact on depression or
distress via the HPPA.
33
This indicates that stress and possible
HPAA hypo-activity could be important factors in particularly
African men’s cardiovascular health, as their vascular responses
predicted progression of sub-clinical atherosclerosis.
The mechanism proposed to be active in the hyperten-
sive men is as follows: the resting high-normal cortisol and
glucose levels and vascular responses due to acute mental stress
could be enhanced via the permissive effect of cortisol on the
catecholamines and subsequently vasoconstriction, inhibiting
insulin production and vasodilating responses.
34-36
The increased
α
-adrenergic responses in hypertensive African men could
enhance progression towards sub-clinical atherosclerosis as well
as the risk for CVD.
37,38
More research in larger sample groups is
clearly needed to confirm these speculations.
A typical
α
-adrenergic vascular pattern was seen in both
genders during stressor application, also suggesting a more
avoidance/passive coping pattern.
37
Alpha-adrenergic responses
are evoked when a person experiences little or no control during
a stressor and is indicative of surrender and feelings of helpless-
ness.
7
These findings could further indicate that Africans feel
overwhelmed and therefore unable to find appropriate solutions
for the problems they face. However, none of the coping styles as
indicated by the normotensive and hypertensive men and women
contributed to the progression of end-organ damage.
Limitations and weaknesses of this study included groups that
were too small when different coping strategies were considered
within the existing blood pressure stratification. Small groups
could have caused the psychological aspect of this study to
lose its strength. An additional stress-related hormone such as
norepinephrine could have clarified the mechanistic approach.
Strengths of the study included the well-controlled psycho-
physiological design of the study as well as the novelty of data
Figure 2a-d: Comparing cardiovascular reactivity values in normotensive (NT) and hypertensive (HT) men (a, b) and
women (c, d) independent of age, BMI and resting BP values. DBP, diastolic blood pressure; Cw, arterial Windkessel
compliance; CO, cardiac output; TPR, total peripheral resistance.
a. Men during cold pressor test, time 1
c. Women during cold pressor test, time 1
b. Men during colour word conflict test, time 1
d. Women during colour word conflict test, time 1
DBP % increase
DBP % increase
DBP % increase
DBP % increase
TPR % increase
TPR % increase
TPR % increase
TPR % increase
Cw % decrease
Cw % decrease
Cw % decrease
Cw % decrease
CO % decrease
CO % decrease
CO % increase
CO % increase
30
20
10
0
–10
–20
40
20
0
–20
40
20
0
–20
–40
100
50
0
–50
a,
p
= 0.05
a,
p
= 0.03
b,
p
= 0.03
a
a
a
a
b
HT
NT
HT
NT
HT
NT
HT
NT
a,
p
= 0.004
a,
p
= 0.03
