Studies in the rat have permitted a complete characterization of the glomerular hemodynamic changes that occur during a normal pregnancy. The rise in glomerular filtration rate (GFR) is the result of an evenly distributed increase in plasma flow to all nephrons due to vasodilation of both pre- and postglomerular resistance vessels. Pregnancy is not associated with any change in blood pressure in the glomerular capillaries; neither is there any detectable alteration in the glomerular water permeability or filtration surface area. Despite the chronically maintained renal vasodilation of pregnancy, gravid rats exhibit substantial renal reserve when challenged with an amino acid load, indicating that a residual renal vasodilatory capacity exists in the kidney of the normal pregnant animal. Despite the concomitant plasma volume expansion of pregnancy, the tubuloglomerular feedback system (a volume regulatory system that modulates GFR) remains fully active in the pregnant rat, suggesting that the plasma volume in pregnancy is not sensed as expanded by this system. The factor(s) that initiates the gestational rise in GFR is currently unknown, although since similar renal hemodynamic changes occur in the pseudopregnant rat, the stimulus is maternal rather than fetoplacental in origin.