Body fluid regulation includes control of intakes and losses. Homeostasis by excretion is provided by the kidney. The signaling pathways linking total body sodium to sodium excretion are ill defined particularly when sodium intakes are high. Two mutually exclusive concepts exist, (i) parallel inputs to the kidney through nervous, hormonal, and physical factors, and (ii) one dominating mechanism ('pressure natriuresis') modulated by said factors. The aim is to evaluate the background of the two concepts. Methodological considerations are crucial. Like temperature control and osmoregulation, sodium homeostasis is sensitive to all forms of stress including anesthesia and must be studied under stress-free conditions. Recently several models, including trained, conscious animals and human volunteers, have provided new information. Perturbations included chronic baroreceptor deactivation (Thrasher, 2005) and activation (Lohmeier & Iliescu, 2011) as well as subtle, acute volume expansion (Bie & Damkjaer, 2010). It is now clear that (i) the assumption of general baroreceptor resetting is invalid (1,2), (ii) chronic baroreceptor activation changes sodium balance by non-pressor, non-nervous pathways, and (iii) trivial volume expansion can drive a robust natriuresis without change in arterial blood pressure (3). In addition, results of recent studies of giraffes question the importance of renal interstitial hydrostatic pressure. When operative, the pressure natriuresis mechanism is dominating; however, the recent results indicate that key assumptions behind its dominating role are weak. Physiological natriuresis seems to be elicited primarily by neurohumoral regulation.

References: 

Bie P & Damkjaer M: Clin.Exp.Pharm.Physiol. (2010) 37: e34-e42. Lohmeier T & Iliescu R: Hypertension, 2011[DOI:10.1161HYPERTENSIONAHA.108. 119859] Thrasher TN: Am.J.Physiol. Regul.Integr.Comp.Physiol. (2005) R819–27.