ABSTRACT
In this paper are discussed reasons to suspect that measurements of serum endothelin levels in women with preeclampsia may not provide accurate estimations of the degree of systemic endothelin receptor activation and reasons to suspect that systemic endothelin receptor saturation studies should provide such estimations more accurately.
Subject(s)
Endothelins/blood , Pre-Eclampsia/blood , Receptors, Endothelin/physiology , Blood Specimen Collection , Capillaries , Elbow/blood supply , Female , Humans , Paracrine Communication , Pregnancy , Reproducibility of Results , Uterus/blood supply , VeinsABSTRACT
Lipid accumulation - in hepatoytes (both subclinically and in acute fatty liver of pregnancy), in the endothelium of placental vessels ("acute atherosis"), and in the bloodstream - has been well established to be a consequence of preeclampsia. Hyperlipidemia (specifically hypertriglyceridemia) has been demonstrated to be a risk factor for the development of preeclampsia. These lipid-related aspects of preeclampsia may appear unrelated, but all are here demonstrated to provide evidence for a causative role for endothelin in the etiology of preeclampsia. Evidence for the potential of endothelin to cause lipid accumulation in hepatocytes and in endothelial cells, by means of activating G protein cascades in these cells, is presented. The capacity of typical free fatty acid constituents of triglycerides to "drive" interacellular G protein cascade-related events is also discussed - which, in this scheme, offers a plausible explanation for hypertriglyceridemia's role as a risk factor for developing preeclampsia. Additional evidence is provided which substantiates endothelin's capacity to cause most of the observed aberrations known to occur in preeclampsia.
