Decreased contractile tension and relaxation to nitroprusside in umbilical and placental arteries and veins in toxemia.

Pre-eclampsia is characterized by hypertension, renal damage and diffuse intravascular coagulation. The mechanism is unknown. However, removal of the placenta restores normal maternal blood pressure. We tested the concept that hyper-reactivity of the placental vessels contributed to the hypertension of pre-eclampsia. Rings of human umbilical artery (UA) and vein (UV), placental artery (PA) and vein (PV), obtained from normal (N) and pre-eclamptic (P) women immediately after delivery, were suspended in a muscle chamber for recording of their stress-strain curves and tension development in response to KCl, U46619 and serotonin (5-HT) and relaxation to sodium nitroprusside (SNP). The incremental elastic moduli (IEM) and maximal tension (dynes/cm2 × 105) and EC50 (μM) were calculated. The IEM for NUA and NUV were between 2 and 9 dynes/cm2 × 105 whereas the IEM for NPA and NPV were between 2 and 16 dynes/cm2 × 105, during changes in strain from 0.1 to 1.2 times the initial diameter. The IEM for PUA and PUV were between 2 and 16 dynes/cm2 × 105 whereas the IEM for PPA and PPV were between 2 and 25 dynes/cm2 × 105 (p<0.05). The contractions of NUV, NUA, NPA and NPV to KCl, 5-HT and U46619 were greater than those obtained in the same vessels from pre-eclamptic women. SNP-induced relaxation was attenuated or non-existent in vessels obtained from pre-eclamptic women. Thus, pre-eclampsia is associated with decreased extensibility, impaired contractility and impaired endothelium-independent relaxation. It is unlikely that enhanced vascular reactivity contributes to the hypertension of pre-eclampsia.