Maternal ET-1 levels are elevated in pregnancy-induced hypertension but may not be the primary cause of blood pressure increase, as ET-1 levels decrease slowly postpartum while blood pressure normalizes quickly.
ET-1 elevation in PIH/PIP is associated with hypertension but may not drive BP rise; leaves open its causal role and therapeutic relevance.
To assess the possible pathophysiological role of endothelin-1 (ET-1) in pregnancy-induced hypertension (PIH), plasma immunoreactive ET-1 levels were consecutively followed at the 3rd trimester, as well as 1 week and 1 month postpartum, in PIH (n=6), pregnancy-induced proteinuria without hypertension (PIP)(n=2), and normal pregnancy (n=7). Before delivery, the ET-1 levels in PIH (4.4±0.5pg/ml) and PIP (4.5±0.6pg/ml) were higher than normal pregnancy (1.5±0.2pg/ml) (p<0.01, p<0.01). The ET-1 level during pregnancy correlated with BP (mean BP; r= 0.69, p<0.01), serum uric acid (r=0.75, p< 0.05), the degree of proteinuria (r=0.62, p<0.05), and ET-1 level in cord venous blood (r=0.58, p< 0.05); in addition, it also tended to correlate with plasma renin activity (r=-0.58, p<0.06). In PIH, BPs were normalized within 1 month after the delivery, whereas the ET-1 level decreased slowly. These results suggest that the maternal ET-1 level was elevated in PIH; however, ET-1 may not be the primary cause of the BP increase. (Hypertens Res 1992; 15: 149-154)
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Ohya et al. (1992) studied this question.
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