Tissue fluid balance, plasma volume regulation and clinical oedema formation are governed by the Starling principle of microvascular fluid exchange. This states that transendothelial filtration is driven by capillary pressure (Pc) and interstitial protein osmotic pressure (πi), while a counteracting absorptive force is exerted by plasma protein osmotic pressure (πp) and interstitial pressure (Pi). SincePc falls along a capillary, the plausible concept of filtration from arterial capillaries and sustained reabsorption into venous capillaries has become embedded in the literature. Most of us learned this as first year undergraduates and took it to be a well proven, somewhat fossilized truth. In recent years, however, this ‘accepted’view has undergone substantial experimental and theoretical re-evaluation; see the Classical Perspective by Michel (2004) in this issue of The Journal of Physiology. In particular, a landmark study of the Pc–filtration relation by Michel & Phillips (1987) demonstrated that although absorption occurs transiently at Pc< πp, absorption cannot be sustained, probably because πi increases with time. A further problem was the ‘low lymph flow paradox’, namely that net capillary filtration rate calculated from tissue-averaged Starling forces (including πi) is much greater than the tissue