Let us see how the afferent and efferent mechanisms operate when salt intake is low.

First, a decrease in salt intake causes a decrease in ECF volume, which stimulates the baroreceptors (afferent mechanisms); then the CNS integrative control center sends a message via the efferent mechanisms to the kidney to conserve Na⁺ and water to restore volume. The mechanisms involved are:

Renin causes the formation of AII, which promotes renal vasoconstriction as well as aldosterone release; the latter stimulates renal tubular reabsorption of Na⁺. Second, increase in SNS (norepinephrine) causes renal afferent and efferent arteriolar vasoconstriction, resulting in a decrease in renal blood flow (RBF) and a slight decrease in GFR. This causes an increase in filtration fraction (GFR/RBF), leading to a decrease in peritubular hydrostatic pressure and an increase in plasma oncotic pressure. These changes in Starling forces favor Na⁺ reabsorption by peritubular capillaries. Norepinephrine also stimulates renin secretion and AII formation. Third, ADH secretion increases, which promotes water reabsorption. Finally, the synthesis of ANP, which promotes excretion of Na⁺, is decreased. The net result is a decrease in Na⁺ excretion and maintenance of Na⁺ and water balance .

When Na⁺ intake increases, the ECF volume also increases. The afferent mechanisms sense this excess ECF volume, and the vasomotor center conveys a message via the efferent mechanisms to restore volume. This is achieved by the inhibition of salt- and water-retaining mechanisms (renin-angiotensin-aldosterone, SNS and ADH) and the activation of salt-losing mechanisms (ANP). Alterations in physical factors also inhibit Na⁺ reabsorption in peritubular capillaries. As a result of these changes, urinary excretion of Na⁺ is promoted to maintain normal volume .