Impaired ATP turnover and ADP supply depress cardiac mitochondrial respiration and elevate superoxide in nonfailing spontaneously hypertensive rat hearts.

@article{Hickey2009ImpairedAT,
  title={Impaired ATP turnover and ADP supply depress cardiac mitochondrial respiration and elevate superoxide in nonfailing spontaneously hypertensive rat hearts.},
  author={Anthony J R Hickey and Chau Chia Chai and S. Y. Thomas Choong and Silvana de Freitas Costa and Gretchen L Skea and Anthony R. J. Phillips and Garth J S Cooper},
  journal={American journal of physiology. Cell physiology},
  year={2009},
  volume={297 3},
  pages={
          C766-74
        }
}
Although most attention has been focused on mitochondrial ATP production and transfer in failing hearts, less has been focused on the nonfailing hypertensive heart. Here, energetic complications are less obvious, yet they may provide insight into disease ontogeny. We studied hearts from 12-mo-old spontaneously hypertensive rats (SHR) relative to normotensive Wistar-Kyoto (WKY) rats. The ex vivo working-heart model of SHR showed reduced compliance and impaired responses to increasing preloads… CONTINUE READING

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