Effects of reduced renal artery pressure on feedback control of glomerular filtration

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Abstract
The rat tubuloglomerular feedback mechanism regulates glomerular filtration rate in response to an increased distal delivery of fluid. It can be modified by changes in body fluid balance mediated via interstitial pressure changes. Whether reduction in arterial perfusion pressure from 115-75 mm Hg would modify feedback sensitivity and activity and, whether a change in feedback sensitivity would affect autoregulation of glomerular filtration rate was investigated. In micropuncture experiments proximal tubule stop-flow pressure was measured while the loop of Henle was perfused at different flow rates, and SNGFR [single nephron glomerular filtration rate] was measured by collecting fluid from both distal and proximal tubules of the same nephron. Maximal change in stop-flow pressure (.DELTA.PSF), loop perfusion rate at which half the .DELTA.PSF was obtained, the turning point (TP), and the difference in proximal and distal measured SNGFR (P-D) were measured to assess the activity of the feedback system. Under control conditions the TP was 23 nl/min and the P-D was 5.4 nl/min. Immediately after aortic constriction, distally measured SNGFR fell 38%. At this time P-D was not different from zero and the TP was not changed. After 20-60 min of reduced arterial pressure, the TP was reduced, and P-D reappeared. Immediately after the clamp was removed, TP remained low, distally measured SNGFR increased by only 14%, and P-D increased further. After blood pressure was returned to normal for more than 20 min, TP and P-D were also normalized. These results indicate that during prolonged clamp and early declamp the feedback mechanism has a high sensitivity and contributes to the reduction of glomerular filtration rate. Autoregulation operates in a lower range of pressures after a prolonged period of hypotension than it does in the normal kidney. The results reveal a slowly adapting mechanism capable of resetting the sensitivity of the feedback control mechanism, and, thus varying the contribution of feedback control to autoregulation of SNGFR.

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