A volume-independent component to postdiuretic sodium retention in humans.

Net sodium (Na) loss during diuretic administration is limited by postdiuretic renal salt retention. This could be a homeostatic response to extracellular fluid volume (ECV) depletion. However, rats infused with loop diuretics develop structural and functional adaptations in the distal nephron that enhance NaCl reabsorption. Therefore, the hypothesis that postdiuretic Na retention in humans contains a volume-independent component was tested. Normal volunteers were equilibrated to a 120 mmol/24 h Na intake. For the first protocol, subjects received, in random order, a placebo, bumetanide (B), or bumetanide accompanied by an infusion of an electrolyte solution at a rate adjusted to match urine flow and thereby to obviate Na losses (bumetanide plus volume replacement; B + VR). After the completion of B diuresis, there was a positive Na balance that restored 70% of the Na loss within 42 h. However, this positive Na balance was prevented by volume replacement (B + VR). For the second protocol, subjects received, in random order, a placebo injection and a 100-mmol NaCl load (P + NaCl) or a bumetanide injection plus volume replacement in addition to a 100-mmol NaCl load (B + VR + NaCl). Over the ensuing 42 h, 94% of the load was eliminated when it was infused alone (P + NaCl). In contrast, only 9% was eliminated when it was given with bumetanide and volume replacement (B + VR + NaCl). It was concluded that postdiuretic Na retention in normal human subjects is due both to ECV depletion and to volume-independent Na retention manifest as an inability to excrete a modest NaCl load.(ABSTRACT TRUNCATED AT 250 WORDS)