The activities of some glycosaminoglycan-degrading enzymes in the wall of the umbilical cord artery and their alteration in edema, proteinuria, hypertension (EPH)-gestosis.

Edema, proteinuria, hypertension (EPH)-gestosis is associated with a premature replacement of hyaluronic acid by sulphated glycosaminoglycans (GAGs), both in the umbilical cord arteries (UCAs) and in Wharton's jelly. This phenomenon may be considered as a sign of premature ageing of the umbilical cord tissues. The decrease in hyaluronic acid content in the UCA was found to be the result of reduced biosynthesis of this substance, whereas an increase in sulphated GAGs-content is rather a result of slower degradation of newly synthesised GAGs. In this study the activities of GAGs-degrading enzymes in normal umbilical cord arteries and those taken from newborns delivered by mothers with EPH-gestosis were compared. It was found that EPH-gestosis results in a significant reduction in the activities of neutral endoglycosidases degrading most of the sulphated glycosaminoglycans (with the exception of heparan sulphate). The activities of exoglycosidases also decrease but to a lesser degree. These alterations are thought to be responsible for EPH-gestosis-associated accumulation of sulphated glycosaminoglycans in the extracellular matrix of the arterial wall. Such remodelling of the arterial wall may affect foetal blood circulation. The significance of these phenomena in the pathological mechanism of EPH-gestosis is discussed.