Enalapril maleate affects 2‐oxoglutarate metabolism in mitochondria from the rat kidney cortex
作者:
Ma. Eliane Merlin,
Annibal P. Campello,
Ma. Lúcia W. Klüppel,
期刊:
Cell Biochemistry and Function
(WILEY Available online 1994)
卷期:
Volume 12,
issue 1
页码: 21-28
ISSN:0263-6484
年代: 1994
DOI:10.1002/cbf.290120104
出版商: John Wiley&Sons, Ltd.
关键词: Enalapril maleate;anti‐hypertensive;liver and kidney cortex mitochondria;oxygen uptake;oxidative phosphorylation;transmembrane potential;2‐oxoglutarate dehydrogenase complex
数据来源: WILEY
摘要:
AbstractEnalapril maleate (EM) is the salt ofN‐{(S)‐1‐(ethoxycarbonyl)‐3‐phenylpropyl}‐L‐alanyl‐L‐proline, used therapeutically as an anti‐hypertensive agent. The effects of EM on some aspects of the energy metabolism and membrane properties of mitochondria from rat liver and kidney cortex were studied, but only the latter were significantly affected. With 0·8 mMof EM and 2‐oxoglutarate as oxidizable substrate for isolated mitochondria from rat kidney cortex, the findings were: (a) inhibition of the respiratory rate in state III (37 per cent) and decrease (45 per cent) in respiratory control ratio (RCR), with only one addition of ADP; (b) reinforcement of the inhibition when a second addition of ADP was made; (c) no significant effect either on the rate of respiration in state IV or on the ADP/O ratio; (d) no effect on the ATPase activity of mitochondria from liver or kidney cortex; (e) inhibition of the transmembrane potential (Δψ) after a second addition of ADP; (f) inhibition of the 2‐oxoglutarate dehydrogenase complex. It is suggested that in kidney mitochondria, EM interferes in the gluconeogenesis dependence of at least five substrates: 2‐oxoglutarate, glutamine, glutamate, lactate, and pyruvate. Also EM may inhibit Na+/H+
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