The syncytiotrophoblast (ST) cell layer of the human villous placenta
expresses nitric oxide (NO) synthase. Because NO is a potent relaxant
of vascular smooth muscle and inhibitor of platelet activity, we postu
lated that exaggerated intervillous aggregation of platelets and reduc
ed fetoplacental blood flow in pre-eclampsia result from reduced expre
ssion of NO synthase (and production of NO) by the ST. Conversion of [
H-3]arginine to [H-3]citrulline and Lineweaver-Burk transformation wer
e used to derive the V-max and K-M of NO synthase, Contrary to our exp
ectations, the V,, was not significantly different between villous pla
centa obtained from nulliparous normal and pre-eclamptic women (n = 11
each). The V-max and K-M were 22.3 +/- 2.3 pmol/mg pet min and 1.3 +/
- 0.1 mu m, and 22.0 +/- 2.7 pmol/mg per min and 1.4 +/- 0.1 mu M, for
villous placenta from the nulliparous normal and pre-eclamptic women,
respectively. The V-max and K-M of placental NO synthase were also co
mparable among multiparous normal and pre-eclamptic women, as well as
women with gestational hypertension. When compared with the enzyme act
ivity of the villous, that of the basal plate was reduced by approxima
tely one-half in all placentae. The calcium-independent activity was c
onsistently 40-fold less than the calcium-dependent activity, and it w
as similar between villous and basal plate, and between placentae from
normal and hypertensive women. We suggest that expression of NO synth
ase is nob different in placentae obtained from normal and pre-eclampt
ic women.