CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
156
AFRICA
significant reference for the pre-eclamptic groups, indicating
that any observations that were common to these groups may
be attributed to the high blood pressure that was a common
characteristic. Therefore if an observation was made in the
pre-eclamptic groups but not the chronic hypertensive group, it
could possibly be attributed to the disease pre-eclampsia.
The lower gestational ages in the early- and late-onset
pre-eclamptic groups in comparison with the normotensive
group may have been as a result of early delivery preventing
further complications, as the only known cure for the syndrome
is delivery of the baby and placenta.
As expected, the systolic and diastolic blood pressure
measurements in the chronic hypertensive and pre-eclamptic
groups were significantly higher than in the normotensive
controls. Interestingly, the systolic and diastolic blood pressures
in the late-onset pre-eclamptic group were significantly higher
than in the chronic hypertensive group, indicating that the
hypertension in late-onset PE may be more severe than that of
chronic hypertension. This may be attributed to the hypertension-
inducing effects of sFlt-1, as previously shown in the murine
model.
19
Recent reports suggest that hypertension in response to sFlt-1
may be associated with increased circulating vascular superoxide
concentrations and that reactive oxygen species could be involved
in mediating the blood pressure response to excessive sFlt-1
during pregnancy. It has been suggested that higher serum sFlt-
1 concentrations could play a role in endothelial dysfunction.
10
The serum VEGF levels in all our groups were below the
detectable limit of the assay, which is to be expected in the
antenatal period
20
and has been shown in previous studies.
21
This
could have been due to the mopping-up effect of the excessive
levels of sFlt-1 that were observed in this study.
Interestingly, the highest level of VEGF mRNA expression
was found in the normotensive group. The level of VEGF
mRNA expression was significantly lower in the late-onset
pre-eclamptic group, and very close to being significantly lower
in the early-onset pre-eclamptic group (
p
= 0.051), compared
with the normotensive group. These findings could also have
been contributing to the VEGF deficiency in the serum of
the pre-eclamptic women. Our study therefore concurs with
previous reports showing evidence of reduced VEGF expression
in the placentae from pregnancies complicated by PE.
22-25
Such
placentae have previously been shown to exhibit morphometric
changes such as altered spiral artery remodelling, deficient
growth and differentiation of terminal villi, and reduced foetal
capillary branching, which could be attributed to reduced VEGF
levels.
26
These studies suggest that VEGF may be implicated in the
molecular mechanisms in abnormal placental development and
is, therefore an important factor involved in the pathogenesis
of PE and its complications. We believe that the relatively high
VEGF mRNA expression in the normotensive group compared
to the pre-eclamptic groups may indicate that VEGF plays a
role in ensuring normal placentation in this group. On the other
hand, an immunohistochemical study showed that VEGF levels
were significantly higher in placental biopsies of patients with
PE than normotensive controls,
27
while other studies reported
no difference in the VEGF mRNA expression levels at term in
placentae from pre-eclamptic and normotensive women.
28,29
We
postulate that the variations could be due to different techniques
used for assessments or to different ethnic populations.
We also observed the circulating level of PlGF to be
significantly higher in the normotensive group compared with the
pre-eclamptic groups. This finding has also been shown by other
workers.
1,30-32
It is well documented that during normal pregnancy,
the levels of PlGF increase but are dramatically reduced post-
partum, since PlGF is produced by syncytiotrophoblast and
extravillous cytotrophoblast cells.
33
However, we did not observe
any significant differences in placental tissue mRNA expression
levels among the four groups. Further studies may help to shed
more light on the control of PIGF levels.
In the present study, the low serum sFlt-1 levels in chronic
hypertensive patients corresponded with the low placental sFlt-
4
3
2
1
0
sFIt-1/VEGF
N
CH EO LO
Fig. 5. Placental mRNA expression levels of sFlt-1/VEGF
in normotensive (N) (
n
= 30), chronic hypertensive (CH)
(
n
= 9), early-onset (EO) (
n
= 8) and late-onset (LO) (
n
= 9)
pre-eclamptic groups.
3.5
3.0
2.5
2.0
1.5
1.0
0.5
0.0
PIGF/GAPDH
N
CH EO LO
Fig. 6. Placental mRNA expression levels of PlGF in
normotensive (N) (
n
= 30), chronic hypertensive (CH)
(
n
= 9), early-onset (EO) (
n
= 8) and late-onset (LO) (
n
= 9)
pre-eclamptic groups.
40
30
20
10
0
AT1/GAPDH
N
CH EO LO
Fig. 7. Mean placental mRNA expression levels of AT1
in normotensive (N) (
n
= 30), chronic hypertensive (CH)
(
n
= 9), early-onset (EO) (
n
= 8) and late-onset (LO) (
n
= 9)
pre-eclamptic groups.
