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• W1977284913 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." @default.
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• W1977284913 date "1999-12-01" @default.
• W1977284913 modified "2023-09-26" @default.
• W1977284913 title "Vascular reactivity in pregnancy and pre-eclampsia" @default.
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• W1977284913 doi "https://doi.org/10.1054/cuog.1999.0040" @default.
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