Under normal steady state conditions, blood volume is a function of dietary salt intake; however, arterial blood pressure (ABP) is not. Therefore, a causal role of ABP in the normal regulation of renal sodium excretion (NaEx) requires operation of an integrative control system together with transient increases in ABP after dietary sodium intakes. Recent evidence indicates that experimental sodium-loading procedures, which simulate dietary situations, increase NaEx without measurable change in ABP. Consequently, the primary signals to the kidney adjusting NaEx after a salty meal are changes in blood composition and/or renal nerve activity. After a dietary sodium intake, blood composition is altered with regard to physical factors other than pressure as well as to specific messengers (e.g. angiotensins and natriuretic hormones). Renal sympathetic nerve activity is altered by changes in blood volume, also by small deviations occurring at constant ABP. At low-salt and high-salt conditions, homeostasis may be established by different control systems. During low-salt conditions, the renin system is dominating. At high-salt diets, many potential mediators may participate (e.g., natriuretic hormones, renal nitric oxide, renal prostaglandins, dopamine, bradykinin, and (other) sodium pump inhibitors). Common to all of these is the absence of a clear homeostatic context. Recent studies of the hierarchy of neurohumoral feed-back systems, which constitute the primary defence against changes in total body sodium, will be reviewed.