PRESSURE NATRIURESIS AND RENAL MEDULLARY BLOOD-FLOW IN DOGS

Citation
Dsa. Majid et al., PRESSURE NATRIURESIS AND RENAL MEDULLARY BLOOD-FLOW IN DOGS, Hypertension, 29(4), 1997, pp. 1051-1057
Citations number
34
Categorie Soggetti
Peripheal Vascular Diseas
Journal title
ISSN journal
0194911X
Volume
29
Issue
4
Year of publication
1997
Pages
1051 - 1057
Database
ISI
SICI code
0194-911X(1997)29:4<1051:PNARMB>2.0.ZU;2-H
Abstract
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.