Nitric oxide synthase expression is increased in endothelial cells exposed to plasma from women with preeclampsia . Davidge, Sandra T., Philip N. Baker, and James M. Roberts. Magee-Womens Research Institute and Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh, Pittsburgh, PA 15213
APStracts 2:0141H, 1995.
Endothelial cell function is proposed to be altered by a factor(s) in the maternal circulation of women with the pregnancy disorder, preeclampsia. Our initial hypothesis was that in preeclampsia, such factor(s) would reduce synthesis of nitric oxide (NO) by endothelial cells. However, we previously observed increased NO synthase activity in endothelial cells exposed to plasma from preeclamptic women. This study tested whether exposing cells to plasma from preeclamptic women increased transcription and/or translation of endothelial NO synthase. Cultured bovine coronary microvascular endothelial cells were exposed to 2 % plasma from patients with preeclampsia and patients with uncomplicated pregnancies. Nitrite production was greater in endothelial cells exposed to plasma from preeclamptic women (8.97 +/- 0.54 vs 6.39 +/- 0.59 nmol nitrites/106 cells/24 hours; P < 0.05). Similarly, endothelial NO synthase mass as measured by Western immunoblotting was significantly increased (20980 +/- 1406 vs 15047 +/- 1003 absorbancy units; P< 0.02). There was no detectable difference in mRNA for endothelial NO synthase. However, Actinomycin (3 [mu]g/ml), a transcription inhibitor, significantly decreased nitrite production only in cells exposed to plasma from preeclamptic women (5.28 +/- 0.52 vs 3.56 +/- 0.36 nmol/106 cells/24 hours, P<0.05) . These findings indicate a regulation of the "constitutive" isoform of NO synthase by factor(s) in the blood of preeclamptic women which may have significance in this pathological condition of pregnancy. 

Received 6 January 1995; accepted in final form 3 April 1995.
APS Manuscript Number H10-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 19 April 1995.