Effects of renal artery pressure on interstitial pressure and Na excretion during renal vasodilation

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Abstract
Renal vasodilation has a marked effect on the pressure-natriuresis relationship. The purpose of this study was to determine the role of renal interstitial hydrostatic pressure (RIHP) in mediating the effect of renal perfusion pressure (RPP) on urinary sodium excretion rate (UNa .ovrhdot.V) in control and vasodilated kidneys. The effects of RPP on UNa .ovrhdot.V and RIHP were determined in dogs under control conditions and during renal vasodilation with acetylcholine (Ach, 2.0 .mu.g .cntdot. kg-1 .cntdot. min-1) or secretin (SEC, 0.025 .mu.g .cntdot. kg-1 .cntdot. min-1). Decreases in RPP in control kidneys from 130 to 60 mmHg decreased UNa .ovrhdot.V from 2.9 .+-. 0.1 to 0.6 .+-. 0.3 .mu.eq/min and fractional excretion of Na (FENa) from 0.15 .+-. 0.08 to 0.06 .+-. 0.04%. These changes were associated with significant reductions in RIHP (8.9 .+-. 0.6 to 5.6 .+-. 1.2 mmHg). In Ach-vasodilated kidneys, reductions in RPP from 130 to 60 mmHg decreased UNa .ovrhdot.V from 149.8 .+-. 52.4 to 0.2 .+-. 0.1 .mu.eq/min and FENa from 3.42 .+-. 1.18 to 0.012 .+-. 0.01%. RIHP decreased from 17.8 .+-. 3.4 to 8.4 .+-. 1.3 mmHg, despite autoregulation of RBF. Renal vasodilation with SEC, which did not affect RIHP, had only a small effect on the relationship between RPP and UNa .ovrhdot.V. These data suggest that RIHP may be playing an important role in mediating the effect of RPP on UNa .ovrhdot.V.