1. The functional capacity of Henle's loop was examined during hypotonic, isotonic and hypertonic extracellular fluid volume expansion. To eliminate a possible role of antidiuretic hormone (ADH) in the alteration of free water excretion, rats with congenital diabetes insipidus were used. The infusion of hypotonic saline resulted in a progressive rise in free water clearance (CH2O) throughout the range of urine flow (V) attained. Similar results were obtained in rats treated chronically with deoxycorticosterone acetate (DOCA). The infusion of isotonic saline (sodium chloride, 154 mmol/l) produced an initial rise in CH2O until V represented 10% of the filtered load, after which CH2O appeared to reach a plateau. The limitation of CH2O was more marked when hypertonic saline was infused. Medullary and papillary non-urea solute (NUS) concentration rose progressively with the increasing concentration of the saline solution infused.
2. The greater fractional sodium excretion (FENa) after acute isotonic and hypertonic volume expansion is probably the result of inhibition of sodium reabsorption in the collecting duct, although inhibition in the ascending limb cannot be entirely excluded. The depression of CH2O as a function of V seen during acute isotonic or hypertonic volume expansion can be attributed in part to enhanced water back-diffusion from the collecting duct consequent to the increasing medullary and papillary interstitial NUS concentration, even in the absence of ADH.
3. Chronic expansion of extracellular fluid volume by DOCA administration did not modify the response to hypotonic saline infusion.