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Intermittency of glomerular activity in man has not been demonstrated (1). Therefore, functional changes in the renal hemodynamics of human subjects generally have been attributed to proportional changes in the flow to all nephrons. Thus, the well-es'tablished decrease of glomerular filtration rate and renal blood flow in chronic congestive failure (2, 3) has been considered a result of inadequate cardiac output and secondary renal vasoconstriction, occurring without reduction in the mass of functioning tubules. Since the decrease in filtration reduces the quantity of electrolyte delivered to tubules normally adapted to handle a larger load (4, 5), it has been postulated that the resulting glomerulo-tubular imbalance contributes significantly to the salt and water retention of congestive failure. Recent studies from this and other laboratories (6, 7) indicate, however, that despite the markedly increased renal A-V oxygen difference, there is a significant reduction in renal oxygen consumption in chronic congestive failure. Although this could represent a diffuse depression of parenchymal metabolism, resulting from generalized renal ischemia and hypoxia, an alternative hypothesis exists. In the light of Trueta's demonstration of an intrarenal vascular shunting mechanism in other species (8), this lower oxygen consumption may reflect an intrarenal diversion of blood away from the cortex, bypassing entire nephrons and thereby diminishing the functional mass of actively metabolizing parenchyma. Such a shunting mechanism would result in a decrease in functioning tubules, proportionate to the reduced filtration, and thus would minimize the role of

THE NATURE OF THE RENAL CIRCULATORY CHANGES IN CHRONIC CONGESTIVE FAILURE AS REFLECTED BY RENAL TUBULAR MAXIMAL FUNCTIONS 12