Rats are an excellent animal model in which to study the changes in renal hemodynamics associated with normal pregnancy. Midterm pregnant rats exhibit a maximal renal vasodilation leading to increases in glomerular filtration rate (GFR) and renal plasma flow (RPF). Micropuncture studies in midterm pregnant Munich-Wistar rats have shown that single-nephron GFR (SNGFR) increases, due entirely to increases in plasma flow and, importantly, glomerular capillary blood pressure (PGC) remains unchanged in normotensive pregnancy, due to parallel and proportionally similar reductions in preglomerular (RA) and efferent (RE) arteriolar resistance. Despite the chronic gestational renal vasodilation, pregnancy in normotensive rats with either normal kidneys or a variety of underlying diseases, causes no adverse changes in renal function, perhaps because the glomeruli are protected from damaging high PGC. In the presence of systemic hypertension, the renal vasodilation of pregnancy could put the maternal kidney at risk of injury due to increases in PGC. There are few renal functional studies in preexisting, essential hypertension, but micropuncture studies in spontaneously hypertensive rats (SHRs) have shown that repetitive pregnancies in SHRs cause no functional impairment. Surprisingly, SHRs demonstrated no gestational renal vasodilation, although gestational decreases in peripheral resistance certainly occur in the SHR. This absence of gestational renal vasodilation may be a protective mechanism; it remains to be determined whether hypertensive states in which renal vasodilation does occur are associated with increased risk to the maternal kidney.