In VitroInteraction of Nonsteroidal Anti-inflammatory Drugs on Oxidative Phosphorylation of Rat Kidney Mitochondria: Respiration and ATP Synthesis

1996 ◽  
Vol 334 (2) ◽  
pp. 303-308 ◽  
Author(s):  
Fábio E. Mingatto ◽  
Antonio C. Santos ◽  
Ségio A. Uyemura ◽  
Maria C. Jordani ◽  
Carlos Curti
Keyword(s):  
Oxidative Phosphorylation ◽  
Rat Kidney ◽  
Atp Synthesis ◽  
Kidney Mitochondria ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Inhibition and uncoupling of oxidative phosphorylation by nonsteroidal anti-inflammatory drugs

1999 ◽  
Vol 57 (7) ◽  
pp. 743-752 ◽  
Author(s):  
Rafael Moreno-Sánchez ◽  
Concepción Bravo ◽  
César Vásquez ◽  
Guadalupe Ayala ◽  
Luis H Silveira ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

STUDIES OF FATTY ACID OXIDATION: 5. THE EFFECT OF DECANOIC ACID ON OXIDATIVE PHOSPHORYLATION

1956 ◽  
Vol 34 (1) ◽  
pp. 1227-1232 ◽  
Author(s):  
P. G. Scholefield
Keyword(s):  
Fatty Acid ◽  
Oxidative Phosphorylation ◽  
Rat Brain ◽  
Fatty Acid Oxidation ◽  
Rat Kidney ◽  
Atp Synthesis ◽  
Decanoic Acid ◽  
Brain Mitochondria ◽  
Acid Oxidation ◽  
Rat Brain Mitochondria

The effects of potassium decanoate on the phosphorylation associated with the oxidation of pyruvate by rat-kidney and rat-brain mitochondria have been investigated. The suggestion that these two processes may be uncoupled from each other in the presence of decanoate has been confirmed. Further, it has been shown that the decanoate-insensitive oxidation of pyruvate by rat-brain mitochondria, occurring in the absence of such stimulating agents as fumarate, is not associated with ATP synthesis. The fumarate-stimulated oxidation of pyruvate by rat-brain mitochondria, which is inhibited by decanoate, is associated with a phosphorylation process which is uncoupled by decanoate. When pyruvate oxidation by rat-kidney or by rat-brain mitochondria is uncoupled from phosphorylation, the extent of uncoupling is proportional to the amount of decanoate added.

scholarly journals Nonsteroidal anti-inflammatory drugs alter vasa recta diameter via pericytes

2015 ◽  
Vol 309 (7) ◽  
pp. F648-F657 ◽  
Author(s):  
Teresa Kennedy-Lydon ◽  
Carol Crawford ◽  
Scott S. Wildman ◽  
Claire M. Peppiatt-Wildman
Keyword(s):  
Rat Kidney ◽  
Tubular Damage ◽  
Endogenous Production ◽  
Primary Mechanism ◽  
Cyclooxygenase 1 ◽  
Vasa Recta ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Prostacyclin Analog

We have previously shown that vasa recta pericytes are known to dilate vasa recta capillaries in the presence of PGE2 and contract vasa recta capillaries when endogenous production of PGE2 is inhibited by the nonselective nonsteroidal anti-inflammatory drug (NSAID) indomethacin. In the present study, we used a live rat kidney slice model to build on these initial observations and provide novel data that demonstrate that nonselective, cyclooxygenase-1-selective, and cyclooxygenase -2-selective NSAIDs act via medullary pericytes to elicit a reduction of vasa recta diameter. Real-time images of in situ vasa recta were recorded, and vasa recta diameters at pericyte and nonpericyte sites were measured offline. PGE2 and epoprostenol (a prostacyclin analog) evoked dilation of vasa recta specifically at pericyte sites, and PGE2 significantly attenuated pericyte-mediated constriction of vasa recta evoked by both endothelin-1 and ANG II. NSAIDs (indomethacin > SC-560 > celecoxib > meloxicam) evoked significantly greater constriction of vasa recta capillaries at pericyte sites than at nonpericyte sites, and indomethacin significantly attenuated the pericyte-mediated vasodilation of vasa recta evoked by PGE2, epoprostenol, bradykinin, and S-nitroso- N-acetyl-l-penicillamine. Moreover, a reduction in PGE2 was measured using an enzyme immune assay after superfusion of kidney slices with indomethacin. In addition, immunohistochemical techiques were used to demonstrate the population of EP receptors in the medulla. Collectively, these data demonstrate that pericytes are sensitive to changes in PGE2 concentration and may serve as the primary mechanism underlying NSAID-associated renal injury and/or further compound-associated tubular damage.

Effect of Mercurial Diuretics Upon Oxidative Phosphorylation in Rat Kidney Mitochondria

1958 ◽  
Vol 192 (3) ◽  
pp. 599-602 ◽  
Author(s):  
Roger L. Greif ◽  
Gloria S. Jacobs
Keyword(s):  
Oxidative Phosphorylation ◽  
Intramuscular Injection ◽  
Rat Kidney ◽  
Isolated Kidney ◽  
Kidney Mitochondria

Administration of large doses of Hg203-labeled chlormerodrin to rats does not lower the P/O ratio of isolated kidney mitochondria. In vitro addition of chlormerodrin will lower the P/O ratio of rat kidney mitochondria, but only in concentrations greater than can be found by measurement of the mitochondrial radiomercury content following intramuscular injection. These techniques fail to demonstrate an in vivo effect of chlormerodrin upon oxidative phosphorylation by rat kidney mitochondria.

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