Capillary oncotic pressure as a modifier for tubuloglomerular feedback

Abstract

Earlier experiments have shown that the sensitivity of the tubuloglomerular feedback mechanism can be reset. To study this resetting the effect of peritubular oncotic pressure on the sensitivity of the tubuloglomerular feedback mechanism was examined. Microperfusion experiments were carried out using Munich-Wistar rats. Proximal tubular stop-flow pressure (SFP) was measured in nephron with a surface glomerulus, upstream to a solid paraffin block, while the downstream segment was perfused with Ringer solution (0-80 nl/min). Peritubular capillaries were perfused near the surface macula densa (100-400 nl/min) with Ringer solution, ultrafiltrate of rat plasma, rat plasma, or remnant of rat plasma after ultrafiltration ([protein] about 10 g/100 ml). SFP at 0 perfusion of the loop of Henle was unchanged compared to control at capillary microperfusion. .DELTA.SFPmax was the maximal reduction in SFP that could be released by the feedback mechanism. Ringer and ultrafiltrate perfusions decreased .DELTA.SFPmax to 2.3 .+-. 0.6 (mean .+-. SE) and 2.2 .+-. 0.5 mmHg (control, 10.4 .+-. 0.9 and 9.4 .+-. 1.1 mmHg), respectively. Remnant perfusion increased .DELTA.SFPmax to 14.3 .+-. 3.1 mmHg (control, 7.0 .+-. 2.3 mmHg), whereas plasma perfusion had no effect on .DELTA.SFPmax, 8.4 .+-. 1.5 mmHg (control, 8.0 .+-. 1.3). The oncotic pressure in the peritubular capillary blood near the macula densa region determined feedback activity, probably by changes in interstitial pressure-volume conditions.