The plasma volume is determined by fluid influx through drinking and outflux by renal excretion. Both fluxes are regulated according to plasma volume and composition through arterial pressure, osmoreceptors and vascular stretch receptors. As to the remaining part of the extracellular volume, the interstitial space, there is no evidence that its volume (IFV), pressure or composition are sensed in such a way as to influence water intake or excretion. Nevertheless, IFV is clearly regulated, often pari passu with the regulation of plasma volume. However, there are many exceptions to parallel changes of the two compartments, indicating the existence of automatic, local mechanisms guarding the net transfer of fluid between plasma and interstitium. Thus, a rise in arterial and/or venous pressure, tending to increase capillary pressure and net filtration, is counteracted by changes in the "Starling forces": hydrostatic and colloid osmotic pressures of capillary blood and interstitial fluid. These "oedemapreventing mechanisms" (A. C. Guyton) may be listed as follows: Vascular mechanisms, modifying capillary pressure or interstitial fluid pressure (IFP). Increased transmural vascular pressure elicits precapillary constriction and thereby reduces the rise in capillary pressure. Counteracts formation of leg oedema in orthostasis. Venous expansion transmits pressure to the interstitium in encapsulated organs (brain, bone marrow, rat tail). Mechanisms secondary to increased net filtration, A rise in IFV will increase IFP, and thereby oppose further filtration. Favoured by lowcompliant interstitium. Reduction of interstitial COP through dilution and/or washout of interstitial proteins. A new steady state depends on increased lymph flow. Increased lymph flow permits a rise in net capillary filtration pressure. Low blood flow and high filtration fraction will increase local capillary COP.