Blood and extracellular fluid volume are maintained within narrow limits despite considerable daily variations in the intake in salt and water. As summarized schematically in Figure 15, the urinary excretion of salt and water responds to changes in blood volume and arterial pressure. Volume-sensitive receptors located predominantly in the cardiac atria and arterial tree sense acute changes in the filling of the blood volume compartment, and urinary sodium excretion is adjusted in response to these detector mechanisms by virtue of alterations in both glomerular filtration rate and tubular sodium reabsorption. The reabsorption of sodium by the tubule responds to changes in extracellular fluid volume as well as to changes in filtered sodium load. Glomerular filtration rate and tubular reabsorption of sodium are influenced importantly by physical properties of the plasma in glomerular and peritubular capillaries and by the composition of the tubular fluid. The renal arterial perfusion pressure is a major factor regulating tubular reabsorption of sodium and water as signalled via changes in renal interstitial hydrostatic fluid pressure. Renal nerves and a variety of systemic and local hormones also influence tubular reabsorption of sodium and water directly by effects on transepithelial sodium transport and/or indirectly by altering renal medullary haemodynamics and the pressure-natriuresis-diuresis relationships. Thus, utilizing a variety of overlapping effector mechanisms that influence renal sodium and water excretion, mammalian organisms have achieved a high degree of stability of body fluid volumes. The fundamental relationship between arterial pressure and renal excretion appears to be the major mechanism which provides for the long-term control of body fluid volume. The sensitivity of the pressure-natriuresis-diuresis relationship is modified by the efferent pathways of the rapid-acting reflex and mechanoreceptor detectors of volume. Working together, these mechanisms provide a remarkable degree of rapid and long-term extracellular and blood volume stability.