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.