Abstract
In erythrocytes, the extrusion of a cellular sodium level load is accomplished by the Ouabain--sensitive Na+/K+ pump and by the furosemide-sensitive Na+/K(+)--cotransport, which operates against the passive sodium permeability. An abnormal low rate of net sodium extrusion by the Na+/K+ cotransport was observed in pre-eclamptic patients. At the molecular level the cotransport abnormality seems to be the consequence of an apparent diminished affinity for intracellular Na+. Normal pregnancy is characterized by a strong increase of Na+/K+ cotransport efflux. No difference could be detected between the passive sodium permeability of erythrocytes from normotensive pregnant patients and from normotensive non-pregnant controls. Pre-eclampsia seems to be associated with a low passive sodium and potassium permeability. The abnormalities of cotransport and red cell deformability in patients with pre-eclampsia might be interpreted as an early sign of impaired microcirculation and increased vascular reactivity.
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