Resetting of tubuloglomerular feedback in acute volume expansion in rats

Loss of sensitivity or "resetting" of tubulo-glomerular feedback has been reported after both acute and chronic volume expansion in rats. In chronic volume expansion due to dietary salt loading, resetting was found to result from the appearance of an inhibitory factor in tubular fluid. The aim of the present study was to test the possibility that resetting after acute isooncotic volume expansion may also be due to such an inhibitor. Rats were acutely volume expanded (4.5% of body weight) by infusion of a solution of fresh plasma and Ringer's solution. Tubuloglomerular feedback activity was assessed in expanded and control animals by measuring early proximal flow (EPF) rate during perfusion of the loop of Henle at varying rates with proximal tubular fluid harvested from the control (control TF) and expanded animals (AVE TF). When loops of Henle in control animals were perfused with control TF at 10, 20 or 40 nl min-1, EPF fell from (mean +/- SD) 29.8 +/- 5.6 at zero loop flow to 27.5 +/- 7.5, 21.1 +/- 4.2 and 15.5 +/- 4.5 nl min-1 gKW-1 respectively. Perfusion at the same rates with control TF in expanded animals reduced EPF from 39.5 +/- 9.6 (at zero loop flow) to 35.9 +/- 11.3, 31.6 +/- 4.3 and 22.9 +/- 6.8 nl min-1 gKW-1 respectively. When loops of Henle in control animals were perfused with AVE TF, EPF fell from 28.6 +/- 9.5 (zero loop flow) to 23.5 +/- 8.6, 19.9 +/- 8.2 and 15.6 +/- 6.5 nl min-1 gKW-1 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)