Autor: |
Junhui Sun, Andrew W. Trafford, DW Eisner, Elizabeth Murphy, Emma J. Radcliffe, Angel Aponte |
Rok vydání: |
2018 |
Předmět: |
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Zdroj: |
Abstracts. |
DOI: |
10.1136/heartjnl-2018-bscr.30 |
Popis: |
The availability of ATP is a limiting factor to cardiac contraction. ATP is predominantly produced by mitochondria via oxidative phosphorylation. Nitric oxide acts as a competitive inhibitor of complex IV and following ischemia, S-nitrosylation has been shown to inhibit complex I activity. Given the established role for nitric oxide in the regulation of oxidative phosphorylation, it is the aim of this study to determine if nitric oxide signalling plays a regulatory role in ATP production in the failing heart. An ovine tachypaced model of heart failure has been used. 4–6 weeks tachypacing resulted in an increase in left ventricular diameter (3.10±0.06 cm to 4.04±0.13 cm, p This study is the first to demonstrate a gross increase in the level of myocardial S-NO, and several specific mitochondrial sites of nitrosylation in heart failure. Future work will investigate the functional consequence of nitrosylation at these sites. |
Databáze: |
OpenAIRE |
Externí odkaz: |
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