FETOPLACENTAL VASCULAR PATHOPHYSIOLOGY IN PREECLAMPSIA. IN: RECENT RESEARCH DEVELOPMENTS IN PHYSIOLOGY

Abstract

Preeclampsia is a syndrome that affects a significant proportion of pregnant women worldwide. The several hypotheses proposed regarding the aetiology of preeclampsia highlight the possibility of a critical role played by the placenta and the multiple molecules released by this organ in the onset of the syndrome. Recent reports suggest that not only the placenta itself but also fetal circulating factors such as lipids, including cholesterol, and the endogenous purine nucleoside adenosine, via activation A2A adenosine receptors, are determinant in this syndrome. Alternatively, maternal pregestational obesity and obesity in pregnancy determines the appearance of preeclampsia, with leptin as a key factor in this phenomenon. In addition, maternal and fetal insulin resistance associated with maternal obesity in pregnancy could result from differential expression of insulin receptor isoforms A and B. Fetoplacental endothelium is a primary target for the action of these factors resulting in endothelial dysfunction. Thus, reduced synthesis and release of nitric oxide and increased plasma levels of adenosine are mechanisms involved in the genesis of preeclampsia. We here summarize these observations and propose potential links between these factors in the aetiology of this syndrome. We highlight the possibility that the placenta and the developing fetus are key elements leading to the onset of preeclampsia. Therapies could include modulation of the serum level of adenosine, cholesterol, insulin, and expression of adenosine and insulin receptors, as well as membrane transporters of nucleosides and cholesterol.