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Abstract
During pregnancy, dramatic changes occur in maternal physiology to accommodate the
growing conceptus. Nowhere are these changes more evident than in the cardiovascular
system. Blood volume and cardiac output increase by 40–50%. These increases have occurred
by the second trimester and remain elevated until after parturition. Blood pressure
throughout pregnancy remains low, secondary to a reduced peripheral resistance. However,
in pre-eclampsia, total peripheral resistance increases, causing the blood pressure
to rise. It has been postulated that the changes in vascular reactivity observed in
both normal pregnancy and pre-eclampsia are caused by alterations in the vascular
endothelium.
All blood vessels within the vasculature are lined by a monolayer of flattened, rhomboid-shaped
cells termed the endothelium. For many years these cells were considered to be a passive
barrier between blood and the underlying vasculature. However, in 1980 Furchgott et
al. demonstrated that if blood vessels were denuded of endothelium they were incapable
of vasorelaxation.1This observation and the development of techniques for cell culture have led to much
research in the field of endothelial cell biology. Endothelial cells offer a unique
interface between the intra-and extra-vascular environment and have a diverse function
in normal physiology and pathology, including the regulation of angiogenesis, immune
responses and inflammation, as well as in the maintenance of vascular tone. This review
will examine the evidence for altered agonist-induced vascular reactivity in pregnancy
and pre-eclampsia, and the mechanisms responsible for these alterations.
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References
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© 1999 Published by Elsevier Inc. All rights reserved.