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Sustained cardiac pressure overload induces mitochondrial dysfunction andapoptosis of cardiomyocytes leading to pathological cardiac hypertrophy and dysfunction.Mitochondrial nitric oxide synthase (NOS) appears to cause uncoupling, which producesreactive oxygen species (ROS) instead of nitric oxide (NO), by a decrease in thecofactor tetrahydrobiopterin (BH4). This study focused on examining the changesin mitochondrial BH4 levels during cardiac pressure overload. Chronic cardiacpressure overload was generated by abdominal aortic banding in rats. Levels ofBH4 and its oxidized form were measured in the mitochondria isolated from theleft ventricle (LV) and the post-mitochondrial supernatants. Chronic aortic bandingincreased blood pressure, and induced cardiac hypertrophy and fibrosis. Notably,the BH4 levels were decreased while its oxidized forms were increased in LV mitochondria,but not in the post-mitochondrial supernatants containing the cytosol and microsome.Anti-neuronal NOS antibody-sensitive protein was detected in the cardiac mitochondria.Moreover, continuous administration of BH4 to rats with pressure overload increasedmitochondrial BH4 levels and reduced cardiac fibrosis and matrix metallopeptidaseactivity, but not cardiac hypertrophy. These findings show the possibility thatNOS uncoupling by decreased cardiac mitochondrial BH4 levels is implicated, atleast in part, in the development of cardiac fibrosis, leading to cardiac dysfunctioninduced by pressure overload.

Decreased cardiac mitochondrial tetrahydrobiopterin in a rat model of pressure overload