Abstract
We have previously shown that pravastatin administered to a well-characterized mouse model of preeclampsia decreases the production of the antiangiogenic sFlt-1 and prevents the associated vascular dysregulation. Endothelial nitric oxide synthase (eNOS) is the enzyme responsible for the production of nitric oxide, one of the most potent vascular smooth muscle relaxants. We hypothesize that pravastatin's action is mediated through eNOS, rather than cholesterol reduction or upregulation of mebrane bound vascular endothelial growth receptor-1 (VEGFR-1).
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