Oxygen Shunt Diffusion in Renal Cortex and Its Physiological Link to Erythropoietin Production

  • H. J. Schurek
Conference paper


Oxygen supply in the kidney is at the brink of oxygen deficiency, though blood flow to the kidney is tremendously high. Some of the reasons for this paradox are the recently demonstrated preglomerular oxygen diffusion shunt [13], which may contribute to the high amount of low cortical p02 values measured by invading electrodes [3, 13] and the construction of the capillary network within the renal cortex, the width of which is defined by the tubular diameters. The analysis of cytochrome aa3, 30% of which is in the reduced form under physiological conditions, as measured by transmission spectrophotometry [1], indicated that 70% of the oxygen-deficient area was in the renal cortex, as only 30% was convertible by furosemide and thereby could mide be attributed to (TAL) segments of Herle’s loop within the outer medulla [5].Within the renal medulla, oxygen shunt diffusion in the vascular bundles is the main reason for oxygen deficiency [11]. This critical oxygen supply may induce an oscillation (OSC) between aerobic and anaerobic energy production, a hypothesis [9] derived from a complementarily observed OSC of proximal tubular pressures [6-8], a phase lag OSC of distal tubular fluid conductivity (Gutsche 1988, personal communication), and from recent experimental evidence for an OSC of the p02 at the renal surface with the same frequency [10], representing an OSC of tubuloglomerular feedback (TGF) activity.


Renal Cortex Oxygen Deficiency Proximal Convoluted Tubule Tubuloglomerular Feedback Erythropoietin Production 
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© Springer-Verlag Berlin Heidelberg 1992

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  • H. J. Schurek

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