These results suggest that Nos3−/− mice phenocopied Oasl1−/− mice with respect to endothelial dysfunction from normal conditions and hyperlipidemia-activated endothelial dysfunction promoted an increase in BP that result from a reduction of eNOS/NO bioavailability in the vasculature of Oasl1−/−Apoe−/− mice. The gene discussed is OASL; the disease is endothelial dysfunction.