The early phase of experimental acute renal failure. IV. The diluting ability of the short loops of Henle.

Experiments were conducted to establish whether diminished solute reabsorption in the loop of Henle during acute renal failure could explain the loss of urinary concentration and participate in generating a tubuloglomerular feedback-mediated reduction in filtration rate. The electrolyte content of the fluid in the ascending limb of the loop of Henle was determined in situ by monitoring its electrical conductivity after propulsion into the distal tubule with a sudden burst perfusion. The value of the minimum electrolyte concentration decreased exponentially with increasing equilibration time, reaching a steady-state value equivalent to 27 +/- 9 mM NaCl in normal kidneys, 34 +/- 15 mM in mercuric chloride kidneys and 53 +/- 22 mM following ischaemia. A mathematical model was derived to describe the process of sodium chloride dilution from which it was possible to calculate both the permeability and transport velocity of the cortical thick ascending limb. In the normal kidney, the transport velocity was calculated to be 4.65 +/- 0.92 . 10(-5) cm/s, a value not significantly different from that of the mercuric chloride of ischaemic kidneys, and the estimated permeability was 1.13 +/- 0.52 . 10(-5) cm/s, not different from that of the mercuric chloride kidneys but significantly lower than that calculated for the ischaemic kidneys. It is concluded that for the more severely damaged ischaemic model, the loss of urinary concentrating ability was accompanied by a reduction in diluting ability of the ascending limb of the short loop of Henle, which appears to be due, at least in part, to an elevation of the passive permeability to sodium chloride in this segment.