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We hypothesized that the Dahl salt-sensitive (S) rat, a genetic model of hypertension and kidney disease, is a spontaneous model of superimposed preeclampsia. The Dahl S was compared with the Sprague-Dawley (SD) rat, a strain with a well-characterized normal pregnancy, and the spontaneously hypertensive rat (SHR), a genetic model of hypertension that does not experience a preeclamptic phenotype despite preexisting hypertension. Mean arterial pressure (MAP, measured via telemetry) was elevated in the Dahl S and SHR before pregnancy, but hypertension was exacerbated during pregnancy only in Dahl S. In contrast, SD and SHR exhibited significant reductions in MAP consistent with normal pregnancy. Dahl S rats exhibited a severe increase in urinary protein excretion, glomerulomegaly, increased placental hypoxia, increased plasma soluble fms-like tyrosine kinase-1 (sFlt-1), and increased placental production of tumor necrosis factor-\u03b1 (TNF-\u03b1). The Dahl S did not exhibit the expected decrease in uterine artery resistance during late pregnancy in contrast to the SD and SHR. Dahl S pups and litter sizes were smaller than in the SD. The Dahl S phenotype is consistent with many of the characteristics observed in human superimposed preeclampsia, and we propose that the Dahl S should be considered further as a spontaneous model to improve our understanding of the pathogenesis of superimposed preeclampsia and to identify and test new therapeutic targets for its treatment. <\/jats:p>","DOI":"10.1152\/ajpregu.00377.2014","type":"journal-article","created":{"date-parts":[[2015,4,22]],"date-time":"2015-04-22T23:02:10Z","timestamp":1429743730000},"page":"R62-R70","source":"Crossref","is-referenced-by-count":92,"title":["The Dahl salt-sensitive rat is a spontaneous model of superimposed preeclampsia"],"prefix":"10.1152","volume":"309","author":[{"given":"Ellen E.","family":"Gillis","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jan M.","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of 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