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Modern concepts of renal physiology are based on the assumption that, at least in normal subjects without impotent or aglomerular tubules, nearly all the blood goes first through the glomeruli before reaching the peritubular capillaries (1). Therefore, blood supplying the tubular system is thought to come entirely from the efferent arterioles. Anatomists have described almost every kind of anastomosis, however, which could shunt various parts of the functioning parenchyma (2). Except by Spanner (3), little consideration has been given to their possible significance in the normal kidney (4-6). Likewise, very little is known of the role of renal lymphatic vessels in the function of the kidneys (7, 8). The recent work of Trueta, et al. (9) aroused general interest in this subject, because for the first time 3 an attempt was made to demonstrate the importance of renal vascular channels which bypass the cortex. Although these authors offer only morphological evidence and employ rather vigorous methods (crushing a limb, very large doses of epinephrine, etc.), they were able to show under these conditions a shift between cortical and medullary blood flow in the rabbit. Therefore, it seemed rewarding to investigate whether a similar phenomenon occurs in human subjects and dogs under normal or pathological circumstances, and whether, as Trueta indicated, this is related to the presence of arterial hypertension. The experiments here reported were made in order to detect, if possible, any changes in the relative blood supply of the different parts of the nephron after administration of certain drugs in pharmacologically active

CAN VASCULAR SHUNTING BE INDUCED IN THE KIDNEY BY VASOACTIVE DRUGS? 1