“…This does not, of course, imply that there is no intrinsic tubular mechanism for sodium transport which may be influenced by the character and flow of tubular urine, as has been pointed out (22,24). However, such observations as the failure of a sulfate diuresis to sweep out sodium chloride (25,26), the variable response to urea loads (1,2,6,23), and the cutback in sodium excretion in some diabetic patients despite continued massive glycosuria (18,27,28), suggest that the osmotic influence of the injected solute within the renal tubule may be only one of several determinants. This view is, on the whole, consonant with that expressed in greater detail by Wolf (29).…”