Pressure Natriuresis and Renal Medullary Blood Flow in Dogs

In the present study, we evaluated the effects of changes in arterial pressure on regional renal blood flows and sodium excretion in anesthetized dogs during control conditions and after 5% volume expansion with isotonic saline. Medullary and cortical blood flow responses were determined with laser-Doppler needle flow probes inserted into the midmedullary and midcortical regions, and whole-kidney blood flow was assessed with an electromagnetic flow probe. Volume expansion in six dogs caused marked increases in urine flow (20.2 +/- 5.5 to 82.5 +/- 22.7 micro Liter [center dot] min [center dot] g) and sodium excretion (3.2 +/- 0.5 to 11.1 +/- 2.7 micro mol [center dot] min [center dot] g), with slight increases in glomerular filtration rate (0.92 +/- 0.03 to 1.01 +/- 0.02 mL [center dot] min [center dot] g) but no significant changes in total renal blood flow (4.7 +/- 0.3 to 5.2 +/- 0.6 mL [center dot] min [center dot] g), medullary blood flow (+ 6 +/- 9%), or cortical blood flow (+ 12 +/- 10%). During stepwise reductions in renal arterial pressure (150 to 75 mm Hg) elicited with a renal arterial occluder, both before and after volume expansion, medullary, cortical, and total renal blood flows as well as glomerular filtration rate exhibited efficient autoregulation, with slopes not significantly different from zero over this range of arterial pressure. There were marked increases in the slopes of the relationships between arterial pressure and urine flow (0.18 +/- 0.05 to 0.78 +/- 0.27 micro Liter [center dot] min [center dot] g [center dot] mm Hg) as well as sodium excretion (0.03 +/- 0.004 to 0.10 +/- 0.03 micro mol [center dot] min [center dot] g [center dot] mm Hg ()) during volume expansion. These data demonstrate that medullary blood flow is efficiently autoregulated in dogs during control and volume-expanded states and indicate that the mechanism responsible for the arterial pressure-induced changes in sodium excretion does not depend on coincident alterations in medullary blood flow. (Hypertension. 1997;29:1051-1057.)