Endogenous Na+, K+-ATPase Inhibitors
Evidence began to mount during the 1960s for the existence of an endogenous regulator of sodium transport. De Wardener demonstrated that extracellular fluid volume (ECFV) expansion by saline infusion in dogs produced a marked increase in urinary sodium excretion (1). He showed that this was due to the presence of a circulating factor because blood from a ECFV-expanded dog could induce natriuresis in a recipient dog. The involvement of all known regulators of sodium and water balance was excluded, and de Wardener suggested that the circulating factor was the “natriuretic hormone.” Such a factor could act by inhibiting renal Na+, K+-ATPase, thus inhibiting active reuptake of sodium with a resultant increase in urinary sodium.
KeywordsPosterior Pituitary ATPase Inhibitor Urinary Sodium Excretion Extracellular Fluid Volume Aortic Strip
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