Nitric oxide and pregnancy.
Sladek, Stephen M., Ronald R. Magness, Kirk P. Conrad.
Magee-Womens Research Institute and Department of Obstetrics,
Gynecology, and Reproductive Sciences, University of Pittsburgh,
Pennsylvania 15213; Departments of Obstetrics and Gynecology,
Perinatal Research Laboratories, and Meat and Animal Science,
University of Wisconsin, Madison, WI 53715
APStracts 3:0388R, 1996.
This review will consider whether nitric oxide (NO) contributes to
maternal systemic vasodilation during pregnancy, regulates uterine
and fetoplacental blood flow, and is involved in uterine quiescence
prior to parturition. Also, whether a deficiency of NO contributes to
the hypertensive disorder of pregnancy, preeclampsia, will be
considered. The biosynthesis of NO increases in gravid rats and
sheep, but the status in normal human pregnancy and preeclampsia is
controversial. NO contributes to maternal systemic vasodilation and
reduced vascular reactivity during normal pregnancy; however, the
relative contribution of NO is variable depending on the animal
species, vascular bed, and vessel size. Impaired relaxation responses
to acetylcholine, but not bradykinin or NO donors are observed in
small arteries from women with preeclampsia, suggesting a receptor or
signal transduction defect, although NO may play little, if any role
here. Uterine arteries have increased endothelial nitric oxide
synthase (NOS) activity, protein expression, and cGMP production
during pregnancy, yet whether these mediate uterine vasodilation
during pregnancy remains to be established. NOS is expressed in the
human placental syncytiotrophoblast, and in the fetoplacental and
umbilical vascular endothelium where basal production of NO
contributes to low fetoplacental vascular resistance. Controversy
exists over the status of placental NOS in preeclampsia, although an
abnormality of umbilical NOS activity is likely. Finally, the uterus
has NOS activity which decreases at the end of gestation, and
exogenous NO relaxes the myometrium, but whether endogenous NO
contributes to uterine quiescence during pregnancy has yet to be
confirmed.
Received 13 June 1996; accepted in final form 16 October 1996.
APS Manuscript Number R325-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996