In this laboratory, dogs acutely saline-loaded to 7–8% body weight and treated with large doses of antidiuretic hormone and deoxycorticosterone acetate will excrete on the average 400–700 μequiv/min of sodium. We have been able to study five dogs, similarly treated, which for no apparent cause showed a trivial natriuretic response following comparable volume expansion. Postexpansion sodium excretion varied from 30 to 150 μequiv/min. Glomerular filtration rate and arterial blood pressure remained constant, but in each case p-aminohippurate clearance rate (CPAH) fell in response to acute saline loading. Renal vasodilatation with acetylcholine and elevation of perfusion pressure with noradrenaline reversed the sodium retention. Fractional reabsorption in the proximal tubule was normal, and the loop of Henle appeared to be the major nephron site responsible for the augmented sodium reabsorption. Constancy of arterial blood pressure, fall in CPAH, and response to altered intrarenal hemodynamics seem to characterize these saline-loaded dogs with minimal sodium excretion as a unique population.