Vasodilator factors in the systemic and local adaptations to pregnancy
Open Access
- 31 July 2009
- journal article
- review article
- Published by Springer Science and Business Media LLC in Reproductive Biology and Endocrinology
- Vol. 7 (1), 79
- https://doi.org/10.1186/1477-7827-7-79
Abstract
We postulate that an orchestrated network composed of various vasodilatory systems participates in the systemic and local hemodynamic adaptations in pregnancy. The temporal patterns of increase in the circulating and urinary levels of five vasodilator factors/systems, prostacyclin, nitric oxide, kallikrein, angiotensin-(1–7) and VEGF, in normal pregnant women and animals, as well as the changes observed in preeclamptic pregnancies support their functional role in maintaining normotension by opposing the vasoconstrictor systems. In addition, the expression of these vasodilators in the different trophoblastic subtypes in various species supports their role in the transformation of the uterine arteries. Moreover, their expression in the fetal endothelium and in the syncytiotrophoblast in humans, rats and guinea-pigs, favour their participation in maintaining the uteroplacental circulation. The findings that sustain the functional associations of the various vasodilators, and their participation by endocrine, paracrine and autocrine regulation of the systemic and local vasoactive changes of pregnancy are abundant and compelling. However, further elucidation of the role of the various players is hampered by methodological problems. Among these difficulties is the complexity of the interactions between the different factors, the likelihood that experimental alterations induced in one system may be compensated by the other players of the network, and the possibility that data obtained by manipulating single factors in vitro or in animal studies may be difficult to translate to the human. In addition, the impossibility of sampling the uteroplacental interface along normal pregnancy precludes obtaining longitudinal profiles of the various players. Nevertheless, the possibility of improving maternal blood pressure regulation, trophoblast invasion and uteroplacental flow by enhancing vasodilation (e.g. L-arginine, NO donors, VEGF transfection) deserves unravelling the intricate association of vasoactive factors and the systemic and local adaptations to pregnancy.Keywords
This publication has 135 references indexed in Scilit:
- Hypertension in Response to Chronic Reductions in Uterine Perfusion in Pregnant RatsHypertension, 2008
- Autoantibodies to the Angiotensin Type I Receptor in Response to Placental Ischemia and Tumor Necrosis Factor α in Pregnant RatsHypertension, 2008
- Renin‐angiotensin system revisitedJournal of Internal Medicine, 2008
- Activation of Local Chorionic Villi Angiotensin II Levels But Not Angiotensin (1-7) in PreeclampsiaHypertension, 2008
- Angiotensin-(1-7) Through Receptor Mas Mediates Endothelial Nitric Oxide Synthase Activation via Akt-Dependent PathwaysHypertension, 2007
- Angiotensin II Stimulates Endothelial NO Synthase Phosphorylation in Thoracic Aorta of Mice With Abdominal Aortic Banding Via Type 2 ReceptorHypertension, 2006
- VEGF receptor signalling ? in control of vascular functionNature Reviews Molecular Cell Biology, 2006
- Placental nitric oxide synthase (NOS) activity and nitric oxide (NO) production in normal pregnancy, pre-eclampsia and eclampsiaInternational Journal of Gynecology & Obstetrics, 2001
- Angiotensin-(1–7) Augments Bradykinin-Induced Vasodilation by Competing With ACE and Releasing Nitric OxideHypertension, 1997
- MATERNAL VASCULAR PROSTACYCLIN ACTIVITY IN PRE-ECLAMPSIAThe Lancet, 1980