The changes in renal function observed in congestive heart failure include altered pressures and flows and increased reabsorption of sodium and water leading to expanded extracellular fluid volume. These renal effects are mediated by a variety of volume and pressure sensors that stimulate various effectors which act on the kidney. The role of these sensors and effectors, the relationship between left ventricular function (LVF) and urinary sodium excretion (UNaV) and the role of angiotensin II in mediating the renal hemodynamic changes are reviewed. Rats with experimentally induced myocardial infarction (MI) were studied 3 weeks after infarction. Although UNaV decreased as LVF worsened, the decrease in UNaV was evident even in rats with MI and minimal LVF impairment. Infusion of teprotide (an inhibitor of angiotensin I converting enzyme) returned the hemodynamic parameters to or toward values seen in rats without MI, thereby documenting an important role for angiotensin II in congestive heart failure.