“…Last, attempts has been made to produce animal models for preeclampsia, but most are imcomplete compared to the full spectrum of the human disease (14). However, some or most clinical signs can be produced in laboratory animals by uteroplacental hypoperfusion, dietary manipulation, alterations in endothelial function (nitric oxice synthesis inhibition, lowdose endotoxin infusion) and gene manipulation (14,15). Administration of sFlt1 (soluble fms-like tyrosine kinase 1) to pregnant rats induces hypertension, proteinuria, and glomerular endotheliosis, the classic lesion of preeclampsia (16).…”