During normal pregnancy, an early, marked, and sustained increase occurs in glomerular filtration rate (GFR) secondary to renal vasodilation. An optimal increase in GFR is a good predictor of pregnancy outcome. The pregnant rat provides an excellent model of the gestational renal hemodynamic response, and invasive studies in this species have extended our understanding of the glomerular hemodynamic mechanisms involved. Of note, the chronic renal vasodilation of pregnancy is not associated with glomerular hypertension, and pregnancy has no long-term injurious effects when kidney function is normal. The renal vasodilatory response to pregnancy is robust and persists in a range of mild renal diseases and in renal transplant recipients. When maternal renal function is moderately or severely compromised, however, the renal responses during pregnancy are often attenuated, and pregnancy may also accelerate the course of the renal disease. Studies in the rat have indicated a wide range of possible renal hemodynamic responses to pregnancy in rats with underlying kidney damage, which seem to be disease specific. Irrespective of the renal vascular response to pregnancy, there is no evidence to date suggesting that pregnancy leads to glomerular hypertension.