Enhanced tubuloglomerular feedback during peritubular infusions of angiotensins I and II

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Abstract
Experiments were performed in pentobarbital sodium-anesthetized rats to determine whether increases in intrarenal generation of angiotensin II (ANG II) can enhance the sensitivity of the tubuloglomerular feedback mechanism. Stop-flow pressure (SFP) feedback responses to step increases in late proximal perfusion rate were obtained during control conditions and during simultaneous peritubular capillary infusion of either angiotensin I (ANG I) or ANG II. Infusion of either 10-7 M ANG II or 10-5 M ANG I, at rates (18.3 .+-. 0.9 and 14.8 .+-. 1.5 nl/min, respectively) that did not affect resting SEP, enhanced the magnitude of SFP feedback responses both at a low proximal perfusion rate of 10 nl/min (2.9 .+-. 0.9 vs. 0.3 .+-. 0.2 and 4.5 .+-. 1.0 vs. 0.1 .+-. 0.1 mmHg, respectively) and at proximal perfusion rates (> 30 nl/min) that elicited a maximal feedback response (13.1 .+-. 1.0 vs. 10.1 .+-. 0.7 and 13.5 .+-. 1.6 vs. 9.8 .+-. 0.8 mmHg, respectively). With a higher ANG I infusion rate (20 nl/min), control SFP measured in the absence of distal volume delivery decreased from 39.2 .+-. 0.6 to 12.0 .+-. 2.8 mmHg (n = 18). These effects were blocked when the ANG II receptor antagonist, saralasin (10-5 M, Sar), was added to the infusate. In addition, the magnitude of the maximal SFP feedback response was not altered during infusion of Sar alone or ANG I + Sar. These findings indicate that ANG II, either added or formed de novo beyond the glomerular circulation, can enhance the sensitivity of the tubuloglomerular feedback mechanism.

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