Regulation of Sodium Excretion

Overview
  • The rate of renal sodium excretion is largely regulated by its rate of tubular resorption as it is not secreted and its rate of glomerular filtration is fairly constant. Unlike other solutes, the body does not regulate urinary excretion of sodium based on its ECF concentration. Instead, sodium excretion is largely regulated based on the total extracellular fluid volume as discussed extensively in ECF Volume Regulation. Here we only wish to summarize the segments of the tubule which are involved in sodium resorption and briefly outline the intrinsic and neuroendocrine mechanisms which modulate tubular sodium resorption.
Sodium Transport
  • Sodium is resorbed at every segment of the tubule. The proximal tubule is responsible for nearly two-thirds of total sodium transport. The thin loop of Henle does not contribute significantly to sodium resorption. In contrast, the thick ascending Henle accounts for nearly 25% of sodium resorption while the early distal tubule is responsible for 5% of total sodium transport. The late distal tubule and collecting ducts are responsible for nearly 3% of the remaining sodium resorption.
Sodium Transport Regulation
  • Pressure Natriuresis
    • Possibly the most important regulatory mechanism for sodium excretion is pressure natriuresis, an intrinsic autoregulatory property of the kidneys that yields increased salt and water excretion with rising incoming arterial pressure. The mechanism of pressure natriuresis likely modification of the starling forces in the peritubular capillary transport (See: Pressure Natriuresis).
  • Renin-Angiotensin-Aldosterone System
    • The RAAS System is the dominant neuroendocrine system that controls sodium excretion. Angiotensin II directly enhances tubular sodium resorption at multiple segments by activating the basolateral NaK ATPase throughout the nephron. Angiotensin II also modifies the starling forces of peritubular capillary transport to favor sodium resorption. It does this by stimulating constriction of the renal efferent arterioles, yielding two effects: 1) Reduced peritubular capillary hydrostatic pressure and 2) Boosting the fraction of fluid filtered through the glomerulus, thus raising peritubular oncotic pressure. In addition to these direct effects, Angiotensin II also stimulates secretion of aldosterone, a hormone with its own anti-natriuretic effects.
    • Aldosterone acts on the Principal Cells of the late distal tubule and collecting ducts to boost the numbers of luminal sodium channels as well as directly stimulating the basolateral NaK ATPase. Together, these effects increase the luminal permeability to sodium and increase the electrochemical gradient for sodium resorption.
  • Sympathetic Nervous System
    • The sympathetic nervous system activity has a mild anti-natriuretic effect by directly stimulating proximal tubular sodium resorption. Sympathetic renal fibers also appear to stimulate renin release and thus promote activation of the RAAS system. These effects are discussed in SNS - Renal Effects.
  • Atrial Natriuretic Peptide (ANP)
    • Atrial Natriuretic Peptide has a mild pro-natriuretic effect on the tubules. ANP appears to directly sodium resorption in the late distal tubule and collecting ducts and reduces renin secretion. However, the physiological effects of ANP on sodium regulation are fairly mild.