1. The effect of unilateral renal vasodilatation produced by acetylcholine or bradykinin on free water clearance (CH2O) and free water reabsorption (TcH2O) was investigated in dogs in an effort to localize the site(s) in the nephron where renal vasodilatation inhibits tubular sodium reabsorption.

2. Renal vasodilatation in dogs undergoing water diuresis produced an increase in urinary sodium excretion, urine volume and CH2O. However, for any given level of sodium delivery to the diluting segment of the nephron, CH2O was less during the intrarenal infusion of the vasodilator drugs than during the infusion of hypo-osmotic saline.

3. During renal vasodilatation in hydropenic dogs receiving vasopressin and hyperosmotic saline, TcH2O at a given rate of osmolal clearance was depressed. The effect of bradykinin on TcH2O was greater than that of acetylcholine.

4. The results indicate that renal vasodilatation inhibits sodium reabsorption in the proximal tubule and the diluting segment of the nephron as well. Increased medullary blood flow may play an additional role in the effect of acetylcholine and bradykinin on TcH2O.

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