Cardiovascular Journal of Africa: Vol 23 No 2 (March 2012) - page 47

CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 2, March 2012
AFRICA
101
vasculature to adrenergic activation may therefore be one of the
numerous pathophysiological mechanisms leading to end-organ
damage of some organs following malaria infection.
The reduction in blood pressure (
in vivo
) induced by malaria
parasitaemia is a paradox, with the
in vitro
results showing
enhanced response to contractile agents and reduced relaxation
response to acetylcholine. Since the endothelium-dependent
relaxation was attenuated in malaria, there is a need for further
studies on nitric oxide synthase expression in the blood vessels
with malaria parasitaemia. The augmented vascular responses
we observed may be explained by differences in receptor and
protein expression. A study of such expression could provide
more insight on how they are able to modulate cardiovascular
control mechanisms.
Conclusion
Malarial infection caused a reduction in blood pressure without
affecting the heart rate
in vivo
, whereas there was an enhanced
contractile response and attenuated vasorelaxation
in vitro
. This
can be explained by the complex cardiovascular control mecha-
nisms
in vivo,
which are independent of direct action on vascular
smooth muscle.
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