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Department of Physiology and Biophysics and Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505
Normal pregnancy is associated
with reductions in total vascular resistance and arterial pressure
possibly due to enhanced endothelium-dependent vascular relaxation and
decreased vascular reactivity to vasoconstrictor agonists. These
beneficial hemodynamic and vascular changes do not occur in women who
develop preeclampsia; instead, severe increases in vascular resistance
and arterial pressure are observed. Although preeclampsia represents a
major cause of maternal and fetal morbidity and mortality, the vascular and cellular mechanisms underlying this disorder have not been clearly
identified. Studies in hypertensive pregnant women and experimental
animal models suggested that reduction in uteroplacental perfusion
pressure and the ensuing placental ischemia/hypoxia during late
pregnancy may trigger the release of placental factors that initiate a
cascade of cellular and molecular events leading to endothelial and
vascular smooth muscle cell dysfunction and thereby increased vascular
resistance and arterial pressure. The reduction in uterine perfusion
pressure and the ensuing placental ischemia are possibly caused
by inadequate cytotrophoblast invasion of the uterine spiral arteries.
Placental ischemia may promote the release of a variety of
biologically active factors, including cytokines such as tumor necrosis
factor-
and reactive oxygen species. Threshold increases in the
plasma levels of placental factors may lead to endothelial cell
dysfunction, alterations in the release of vasodilator substances such
as nitric oxide (NO), prostacyclin (PGI2), and
endothelium-derived hyperpolarizing factor, and thereby reductions of
the NO-cGMP, PGI2-cAMP, and hyperpolarizing factor vascular
relaxation pathways. The placental factors may also increase the
release of or the vascular reactivity to endothelium-derived
contracting factors such as endothelin, thromboxane, and ANG II. These
contracting factors could increase intracellular Ca2+
concentrations ([Ca2+]i) and stimulate
Ca2+-dependent contraction pathways in vascular smooth
muscle. The contracting factors could also increase the activity of
vascular protein kinases such as protein kinase C, leading to increased myofilament force sensitivity to [Ca2+]i and
enhancement of smooth muscle contraction. The decreased endothelium-dependent mechanisms of vascular relaxation and the enhanced mechanisms of vascular smooth muscle contraction represent plausible causes of the increased vascular resistance and arterial pressure associated with preeclampsia.
endothelium; vascular smooth muscle; pregnancy; hypertension
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