The overall control of body sodium relies on mechanisms that have close links to blood pressure control and hypertension. The Strauss concept of a basal level of body sodium, below which any available sodium is retained and above which any extra sodium is excreted (at a rate exponentially related to the amount present in the body), has been confirmed in rat studies. Total body sodium, on an average sodium intake, thus consists of basal plus extra: the proportions of these can vary and this makes interpretation of total body sodium difficult. Basal body sodium is, in theory, the level at which delivery of sodium to the distal nephron equals distal reabsorption of sodium. The latter is largely determined by aldosterone and, indeed, basal body sodium is high in primary aldosteronism and low in Addison's disease. The half-life of extra sodium is short in primary aldosteronism and long in Addison's disease: it is also short in some hypertensive subjects but in general lengthens with age. The exact mechanisms involved are still uncertain. Most of this work is based on step reductions in sodium intake. Step increases in sodium intake appear to lead to more complicated adjustment processes, with a delay in commencing excretion followed by some under-damping of the system before a new higher level of body sodium and a new equilibrium of intake and excretion is reached.