Endothelial vasodilator production by uterine and systemic
arteries: ii. effects of pregnancy on nitric oxide synthase
expression.
Magness, Ronald R., Cynthia E. Shaw, Terrance M. Phernetton, Jing
Zheng, and Ian M. Bird.
Department of Obstetrics & Gynecology/Perinatal Research
Laboratories and Meat & Animal Sciences, University of Wisconsin
-Madison, Madison, WI 53715
APStracts 3:0402H, 1996.
Pregnancy is characterized by elevations in uterine, but not omental
artery Nitric Oxide Synthase (NOS) specific activity. Hypothesis:
Increases in NO production during pregnancy are associated with
elevations in protein expression of the constitutive NOS isoform,
endothelial cell NOS (ecNOS) in uterine, but not systemic arteries.
Methods: Arterial NOS specific activity and cGMP production were
tested in pregnant sheep in the presence or absence (+5mM EGTA) of
Ca++. Using Western analysis, ecNOS and neuronal NOS (nNOS)
constitutive isoform expressions were evaluated in intact and denuded
(vascular smooth muscle; VSM) uterine and systemic (omental and
renal) arteries, as well as in isolated endothelium-derived proteins
from nonpregnant and pregnant sheep. Results: Uterine and omental
artery NOS activity and cGMP production were inhibited 75-85% by Ca++
removal. ecNOS was localized only in uterine and systemic artery
endothelium (not VSM) by immunohistochemistry and Western analysis;
nNOS was not detected. Compared to nonpregnant ewes, pregnancy
increased expression of ecNOS in uterine [2.1-4.2 fold
(P<0.0001)] and omental [1.3-2.2 fold (P=0.032)], but not
renal (P=0.1367) artery endothelium; fold increases in uterine
> omental artery. Levels of plasma and urinary cGMP were
elevated (p<0.01) proportionally (1.8-2.0) in pregnant versus
nonpregnant ewes. Conclusions: During pregnancy expression of uterine
artery endothelium-derived (not VSM) ecNOS constitutive isoform is
increased while expression in systemic vessels shows little or no
change.
Received 5 February 1996; accepted in final form 4 September
1996.
APS Manuscript Number H111-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996