“…The reason for this remains obscure. It may be that the variability in the rates of sodium transport, encountered by most workers in this field (Visscher et al, 1944 a and b;Bucher, Anderson, and Robinson, 1950;Curran and Solomon, 1957;Berger, Ranzaki, Homer, and Steele, 1959;Shields, 1965a), obscured any change in the intestinal handling of sodium produced by aldosterone. Another reason may be that just as the effect of mineralocorticoids on the renal excretion of sodium is difficult to demonstrate in acute experiments in a normal dog (Barger, Berlin, and Tulenko, 1958), so also is their action upon the bowel.…”