Tubular reabsorption was inhibited in isolated dog kidneys by the progressive substitution of plasma chloride by sulphate. In the absence of antidiuretic hormone activity, urine output remained unchanged owing to an equivalent decrease in glomerular filtration rate. This equilibrium was demonstrated under conditions of "saline natriuresis" and was not disturbed by furosemide. Although the impairment of glomerular filtration rate was accompanied by a decrease of total renal blood flow, the equilibrium was not disrupted by angiotensin antagonism. Sodium excretion was enhanced by low plasma chloride concentrations in the absence, but not in the presence of furosemide. The results are not compatible with a specific role of osmolality, sodium or chloride concentrations in the tubular fluid in the adjustment of glomerular filtration. Simultaneous changes in blood flow and tubular flow resistances might explain the results. It is suggested that, in contrast to the mechanism of tubulo-glomerular feedback found in individual nephrons of hydropenic animals, this intrarenal mechanism might serve to protect the organism against sodium loss under conditions of high intake.