In the present study, we evaluated the effects of changes in arterial
pressure on regional renal blood flows and sodium excretion in anesthe
tized dogs during control conditions and after 5% volume expansion wit
h isotonic saline. Medullary and cortical blood flow responses were de
termined with laser-Doppler needle flow probes inserted into the midme
dullary and midcortical regions, and whole-kidney blood flow was asses
sed with an electromagnetic flow probe. Volume expansion in six dogs c
aused marked increases in urine flow (20.2 +/ 5.5 to 82.5 +/- 22.7 mu
L min(-1). g(-1)) and sodium excretion (3.2 +/- 0.5 to 11.1 +/- 2.7 mu
mol.min(-1).g(-1)), with slight increases in glomerular filtration ra
te (0.92 +/- 0.03 to 1.01 +/- 0.02 mL.min(-1).g(-1)) but no significan
t changes in total renal blood flow (4.7 +/- 0.3 to 5.2 +/- 0.6 mL.min
(-1).g(-1)), 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 autor
egulation, 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 mu L.min(-1).g(-1).mm Hg-1) as well as sodium
excretion (0.03 +/- 0.004 to 0.10 +/- 0.03 mu mol.min(-1).g(-1).mm Hg
-1) during volume expansion. These data demonstrate that medullary blo
od flow is efficiently autoregulated in dogs during control and volume
-expanded states and indicate that the mechanism responsible for the a
rterial pressure-induced changes in sodium excretion does not depend o
n coincident alterations in medullary blood flow.