Feedback-mediated reduction of glomerular filtration rate during infusion of hypertonic saline

Abstract

An acute rise in plasma sodium concentration from 146 ± 2.6 to 155 ± 1.7 was produced in rats by the intraarterial infusion of 0.6 M sodium chloride (0.25 ml/min for 4 min followed by 0.25 ml/hr). A parallel fall in whole kidney GFR (from 0.45 ± 0.02 to 0.36 ± 0.04 ml/min per 100 g of body wt) and SNGFR measured in the distal tubule (31.4 ± 3.01 to 27.9 ± 2.40 nl/min) was observed. In contrast, proximally measured SNGFR (with feedback interrupted) rose from 32.7 ± 2.73 to 37.1 ± 2.84 nl/min. The loop of Henle flow, determined from distal SNGFR and [TF/P](inulin) in late proximal fluid collected without interrupting tubular flow, rose from 13.7 ± 1.50 to 17.0 ± 1.42 nl/min as a consequence of a fall in proximal reabsorptive rate from 15.8 ± 1.87 to 11.0 ± 1.37 nl/min. Intraarterial infusion of hypertonic sodium bicarbonate resulted in comparable increases in plasma sodium concentration and inhibition of proximal reabsorption but did not produce a fall in filtration rate. The authors conclude (1) acute infusion of hypertonic sodium chloride results in an inhibition of proximal reabsorption and therefore in an increased rate of loop of Henle flow, (2) this increase in flow causes a fall in GFR through the tubuloglomerular feedback mechanism, and (3) acute infusion of hypertonic sodium bicarbonate does not result in a feedback-mediated fall in GFR, presumably because increased delivery of bicarbonate-rich fluid does not activate the feedback mechanism.