The effect of captopril on nitric oxide formation and on generation of radical forms of mitochondrial respiratory chain compounds in ischemic rat heart

Title:

The effect of captopril on nitric oxide formation and on generation of radical forms of mitochondrial respiratory chain compounds in ischemic rat heart

Creator:

Vavřínková, H., Milada Tutterová, Pavel Stopka, Jana Divišová, Ludmila Kazdová, and Zdeněk Drahota

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:28506ff5-6af3-4a4f-8bea-5015d6b36efb
uuid:28506ff5-6af3-4a4f-8bea-5015d6b36efb
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, oxid dusnatý, ischemie, nitric oxide, ischemia, ACE inhibitors, L-arginine, mitochondrial radicals, ischemia-reperfusion injury, heart ischemia, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The increase of radical forms of mitochondrial respiratory chain compounds (MRCC) is an indicator of an increased risk of the formation of oxygen radicals. Using electron paramagnetic resonance (EPR), we found an increase of signals corresponding to ubisemichinone radical (·QH) and ironsulfur proteins radical forms (·FeS) of these respiratory chain compounds during ischemia in the isolated perfused rat heart (·QH increased from 1.51 to 3.08, ·FeS1 from 1.14 to 2.65 arbitrary units). During the 5-min reperfusion, the signals returned to normoxic levels. In isolated mitochondria exposed to anoxia and reoxygenation the radical forms of ·QH and ·FeS2 changed in a similar manner as in the intact heart. A combination of in vivo captopril treatment and in vitro L-arginine administration significantly decreased the levels of MRCC radicals in the isolated myocardium (·QH from 2.61 to 1.72 and ·FeS1 from 1.82 to 0.46 under normoxia; ·QH from 4.35 to 2.66 and ·FeS1 from 1.93 to 1.35 during ischemia). This decrease in MRCC radical forms was associated with increased NO levels in the perfusate, determined as NO2-/ NO3-, as well as tissue NO levels determined using EPR as the dinitrosyl iron complex (DNIC). These results provide new information about the cardioprotective effects of ACE inhibitors and L-arginine., H. Vavřínková, M. Tutterová, P. Stopka, J. Divišová, L. Kazdová, Z. Drahota., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2001 Volume:50 | Number:5

Harvested from:

CDK

Metadata only:

false