Abstract
The pO2 of ureteral urine under osmotic diuresis responds inversely to changes in renal arterial and venous pO2. With a rise in arterial pO2 there is only a transient increase but then a rapid fall in urinary pO2, usually to lower than the initial levels in both anesthetized and unanesthetized dogs. Opposite changes occur when the arterial pO2 is diminished. The renal blood flow falls as arterial pO2 rises with transfer of the animal from air to 100% O2, but the total O2 consumption of the kidney remains unaltered. The most simple and reasonable explanation of these findings postulates the existence of a mechanism sensitive to arterial pO2 for redistribution of medullary blood flow. This does not, however, rule out the possibility that an increase in arterial pO2 might be accompanied by an augmentation of O2 utilization so large as to diminish tissue pO2, and vice versa. If this is true there is, to our knowledge, no analogue in biology and there are several points of evidence against the metabolic hypothesis.
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