Alterations to the balance of angiogenic (i.e., placental growth factor) and anti-angiogenic factors (i.e., soluble fms-like tyrosine kinase 1; soluble endoglin) X-396 order are highlighted as potential contributors to endothelial cell dysfunction. Notably, increased activation of inflammatory cells, with concomitant shifts in cytokine profiles, has been observed in women with preeclampsia. The authors describe these alterations and how they are linked with endothelial cell dysfunction. Investigations that have documented the effect of preeclampsia on altered vasoresponsiveness of both systemic and uterine resistance vessels

are summarized. Recent developments implicate not only circulating factors, but also endothelial-derived microparticles, as mediating the systemic vascular effects of preeclampsia. Endothelial dysfunction within the fetoplacental circulation also is a central feature of GDM. Guzmán-Gutiérrez et al. [6] describe the regulation of l-arginine transport within the macro- and microvascular endothelial cells of the placental circulation, and highlight the inherent phenotypic differences exhibited by these two types of endothelial cells. The authors summarize recent advances in understanding how the placental endothelial cell l-arginine/nitric oxide (NO) signaling pathway is subject to modulation by adenosine and insulin. They discuss a model of how imbalances in adenosine and insulin-mediated signals

may disrupt physiological function of the l-arginine/NO pathway within the placental circulation during GDM. As the rate of occurrence of the pathological condition of GDM grows in the population click here in parallel with rates of obesity and insulin resistance, this undoubtedly is a key area that warrants further investigation. “
“Please cite this paper as: Leach and Mann (2011). Consequences of Fetal Programming for Cardiovascular Disease in Adulthood. Microcirculation 18(4),

253–255. This Spotlight Issue of Microcirculation contains six current perspectives on the role of the intrauterine environment, especially maternal nutritional status and maternal diabetes, in influencing fetal growth and cardiovascular health in the offspring in later life. The reviews address issues such as the existence of a commonality PJ34 HCl of mechanism following both under-nutritional and over-nutritional states in utero; alterations in the placental fetal microcirculation in response to maternal and fetal changes; transmission of metabolic or nutritional perturbations affecting fetal endogenous antioxidant defense pathways; the presence of a disadvantageous microvascular phenotype resulting from perinatal priming; interactions between developmental programming and genetic variation in noncommunicable adult diseases such as hypertension and hypercholesterolemia; and unresolved questions on the independency and causal mechanisms for low birth weight/intrauterine growth restriction and the risk of developing the metabolic syndrome.