Heme oxygenase-derived carbon monoxide promotes arteriolar endothelial dysfunction and contributes to salt-induced hypertension in Dahl salt-sensitive rats.

@article{Teran2005HemeOC,
  title={Heme oxygenase-derived carbon monoxide promotes arteriolar endothelial dysfunction and contributes to salt-induced hypertension in Dahl salt-sensitive rats.},
  author={Federico J Teran and Robert A. Johnson and Blake K Stevenson and Kelly J. Peyton and Keith E Jackson and Scott D Appleton and William Durante and Fruzsina K. Johnson},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2005},
  volume={288 3},
  pages={R615-22}
}
Vascular tissues express heme oxygenase (HO), which metabolizes heme to form carbon monoxide (CO). Heme-derived CO inhibits nitric oxide synthase and promotes endothelium-dependent vasoconstriction. After 4 wk of high-salt diet, Dahl salt-sensitive (Dahl-S) rats display hypertension, increased vascular HO-1 expression, and attenuated vasodilator responses to ACh that can be completely restored by acute treatment with an inhibitor of HO. In this study, we examined the temporal development of HO… CONTINUE READING

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