Determinants of intrarenal oxygenation. I. Effects of diuretics

To study renal cortical and medullary oxygen tensions, we used sensitive Clark-type O2 microelectrodes, inserted by micromanipulators into the cortex and medulla of kidneys of anesthetized rats. As previously reported, under basal conditions, medullary PO2 was significantly lower than cortical PO2....

Full description

Saved in:
Bibliographic Details
Published inThe American journal of physiology Vol. 267; no. 6 Pt 2; p. F1059
Main Authors Brezis, M, Agmon, Y, Epstein, F H
Format Journal Article
LanguageEnglish
Published United States 01.12.1994
Subjects
Absorption
Acetazolamide - pharmacology
Animals
Bumetanide - pharmacology
Diuretics - pharmacology
Ethacrynic Acid - pharmacology
Furosemide - pharmacology
Kidney - metabolism
Kidney Cortex - blood supply
Kidney Cortex - metabolism
Kidney Medulla - blood supply
Kidney Medulla - metabolism
Mannitol - pharmacology
Microelectrodes
Oxygen Consumption - drug effects
Rats
Rats, Sprague-Dawley
Online AccessGet more information

Cover

More Information
Summary:To study renal cortical and medullary oxygen tensions, we used sensitive Clark-type O2 microelectrodes, inserted by micromanipulators into the cortex and medulla of kidneys of anesthetized rats. As previously reported, under basal conditions, medullary PO2 was significantly lower than cortical PO2. Furosemide, which inhibits reabsorptive transport in the medullary thick ascending limb, increased medullary PO2 from 16 +/- 4 to 35 +/- 4 mmHg (P < 0.0005) without altering cortical PO2. This effect, reproduced by ethacrynic acid and bumetanide, was selective for loop diuretics and was directly due to decreased tubular O2 consumption, since medullary blood flow was remarkably reduced by furosemide (-28 +/- 6% from baseline, P < 0.0001, as measured by a laser-Doppler probe). By contrast, acetazolamide, which decreases proximal tubule metabolism, selectively increased cortical PO2. These data are, in general, consistent with tubular metabolism as a major determinant of intrarenal oxygenation and suggest, in particular, that medullary reabsorptive work is at least in part responsible for renal medullary hypoxia.
ISSN:0002-9513