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Pressure Natriuresis

  • Pressure Natriuresis appears to be the dominant physiological mechanism that connects changes in the systemic arterial pressure to changes in total body sodium amount. Pressure natriuresis acts by increasing renal sodium excretion when incoming arterial pressure to the kidneys rises. The mechanism operates completely autonomously within the kidneys and independently of any external neurohormonal regulatory mechanisms. Its importance in connecting renal sodium transport to arterial pressure renders pressure natriuresis the dominant mechanism of both ECF Volume Regulation and Systemic Arterial Pressure - Long-term Regulation.
  • The mechanism of pressure natriuresis is not completely understood but changes in the peritubular capillary transport likely underlie its operation. As incoming arterial pressure to the kidneys increases, the hydrostatic pressure within the peritubular capillaries also increases. This reduces the starling force for fluid resorption into the capillaries from the renal interstitial fluid. With reduced peritubular capillary resorption, water and salt appear to backleak into the tubule, yielding enhanced urinary sodium excretion.
  • The relationship between incoming arterial pressure and renal urinary sodium excretion in an isolated kidney is rather gradual and thus pressure natriuresis alone cannot account for the precision in ECF volume regulation which is normally observed. It appears that the Renin-Angiotensin-Aldosterone System (RAAS) is responsible for rendering pressure natriuresis much more sensitive to responses in arterial pressure. Consequently, pressure natriuresis modulated by the RAAS is likely the basis of long-term ECF volume and systemic arterial pressure regulation.
  • The ingestion of large loads of sodium occurs frequently in a modern diet. This sodium is rapidly added to the ECF by the alimentary tract, resulting in a slight increase in ECF osmolarity to which processes of ECF osmoregulation respond by inducing a thirst instinct. The resultant addition of free water, combined with the previous load of sodium lead to an expansion of ECF volume that in a normal individual slightly increases the systemic arterial pressure. The increased incoming arterial pressure to the kidneys triggers the pressure natriuresis phenomenon which leads to enhanced urinary excretion of salt and water, returning the ECF volume and thus arterial pressure to levels prior to the sodium load.