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Endothelin (ET) is a potent vasoconstrictor peptide. In this study, we investigated maternal venous plasma ET levels measured by Sandwich-enzyme immunoassay within a week before the onset of labor, and measured plasma renin activity and plasma aldosterone concentration by radioimmunoassay in normal and severely preeclamptic pregnancies. Also, we determined umbilical cord blood pH and gas concentrations after spontaneous vaginal deliveries and cesarean sections. There was a significant (p < 0.01) negative correlation between maternal ET levels within 1 week before the onset of labor and birth weights. There was no significant correlation between maternal ET levels and umbilical gas concentrations. These data suggest that the correlation is the result of decreasing uteroplacental blood flow. We speculate that increased maternal ET expresses not only maternal renal vascular endothelial injury but also other vascular endothelial injuries. These vascular injuries may occur at least 1 week before the clinical manifestation in the preeclamptic mothers and their fetuses.

Collagen IV is the main collagenous component localized in the trophoblast and glomerular basement membrane. Serum collagen V reflects degradation of basement membrane collagen. In this study, we measured collagen IV levels in maternal serum, umbilical cord serum and amniotic fluid, both from preeclamptic and normal pregnant women, by radioimmunoassay. The serum collagen IV levels in the preeclamptic group were significantly (p < 0.05) higher than those in the normal pregnant group. The amniotic fluid collagen IV level at term was found to be higher than maternal serum collagen IV. We postulate that collagen IV may have an important role in the maintenance of pregnancy. There was a significant positive correlation between maternal serum collagen IV levels and serum laminin levels. There was no significant correlation between maternal serum collagen IV level and blood pressure, urinary protein concentration, or any other laboratory data. These results suggest that there is early damage of endothelial cells in preeclampsia.

Brain natriuretic peptide (BNP) was increased in many hypertensive subjects. In this study, we have evaluated maternal, umbilical plasma and amniotic fluid BNP and atrial natriuretic peptide (ANP) in 19 normotensive pregnant women and in 35 preeclamptic patients. The maternal plasma and umbilical cord plasma ANP (p < 0.05) and BNP (p < 0.005) levels were significantly higher than those in normal pregnancy. There was no significant correlation among ANP level, BNP level, clinical symptoms and laboratory examinations. It is suggested that ANP and BNP may be rather a sequel to preeclamptic pathophysiological changes, and may not play an important role as the etiological factor of preeclampsia.

Laminin is a large noncollagenous glycoprotein localized in the trophoblast and glomerular basement membrane. We measured laminin levels in maternal serum, umbilical cord serum and amniotic fluid, both from preeclamptic and normal pregnant women, by enzyme immunoassay. The serum laminin levels in the preeclamptic group were significantly (p < 0.05 to p < 0.01) higher than those in the normal pregnant group. It has been suggested that laminin plays an important role in implantation of the placenta during early pregnancy. In this study, the amniotic-fluid laminin level at term was found to be lower than maternal serum laminin. We postulate that laminin may not have an important role in the maintenance of late pregnancy. There was a significant positive correlation between maternal serum laminin levels and serum uric acid levels. There was no significant correlation between maternal serum laminin level and blood pressure, urinary protein concentration, or any other laboratory data. These results suggest that there is damage of glomerular and placental spiral arteries in preeclampsia.

To clarify the possible role of elevated atrial natriuretic peptide (ANP) in the pathophysiology of preeclampsia, we measured ANP, renin activity (PRA), angiotensin II (Ang II), TXB2 (a stable metabolite of TXA2) and 6-keto-PGF1 alpha (a stable end product of PGI2) concentrations in the plasma of 19 normal pregnant women and 35 severe preeclamptic patients at term. Plasma ANP levels in the preeclamptic patients (n = 35, 71.5 +/- 3.8 pg/ml, mean +/- S.E.) and also umbilical plasma ANP (n = 35, 83.0 +/- 4.2 pg/ml) were significantly (p less than 0.01) higher than those of normal pregnant women plasma (n = 19, 58.7 +/- 3.7 pg/ml) and umbilical plasma (n = 19, 47.6 +/- 4.7 pg/ml). There was a significant (p less than 0.01) positive correlation between maternal ANP levels and fetal ANP levels (n = 54, r = 0.44). Plasma PRA and 6-keto-PGF1 alpha levels in preeclampsia were significantly (p less than 0.05) lower than those of normal pregnancy. The ratio of 6-keto-PGF1 alpha/TXB2 in preeclampsia was significantly (p less than 0.01) lower than that of normal pregnancy as we reported previously. There was no significant correlation between plasma ANP level and plasma PRA, Ang II, plasma TXB2 and 6-keto-PGF1 alpha concentrations. Moreover there was no significant correlation between plasma ANP level and the severity of preeclampsia. These data suggest the possibility of a transplacental crossing of ANP secreted by feto-placental unit, which might be, at least in part, responsible for the high ANP levels observed in preeclampsia. The ANP in preeclampsia is not related directly to hypertension, but it may play a substantial role in the regulation or normalization of blood volume and vascular reactivity.