Glomerular filtration rate (GFR) and renal plasma flow (RPF) increase by 40-65% and 50-85%, respectively, during normal pregnancy in women. Studies using the gravid rat as a model have greatly enhanced our understanding of mechanisms underlying these remarkable changes in the renal circulation during gestation. Hyperfiltration appears to be almost completely due to the increase in RPF, the latter attributable to profound reductions in both the renal afferent and efferent arteriolar resistances. The major pregnancy hormone involved is relaxin. The mediators downstream from relaxin include endothelin (ET) and nitric oxide (NO). New evidence indicates that relaxin increases vascular gelatinase activity during pregnancy, thereby converting big ET to ET(1-32), which leads to renal vasodilation, hyperfiltration, and reduced myogenic reactivity of small renal arteries via the endothelial ET(B) receptor and NO. Whether the chronic volume expansion characteristic of pregnancy contributes to the maintenance of gestational renal changes requires further investigation. Additional studies are also needed to further delineate the molecular basis of these mechanisms and, importantly, to investigate whether they apply to women.