Mineralocorticoid accelerates transition to heart failure with preserved ejection fraction via "nongenomic effects".

@article{Mohammed2010MineralocorticoidAT,
  title={Mineralocorticoid accelerates transition to heart failure with preserved ejection fraction via "nongenomic effects".},
  author={Selma F. Mohammed and Tomohito Ohtani and Josef Korinek and Carolyn S P Lam and Katarina Larsen and Robert D. Simari and Maria L. Valencik and John C. Burnett and Margaret M. Redfield},
  journal={Circulation},
  year={2010},
  volume={122 4},
  pages={370-8}
}
BACKGROUND Mechanisms promoting the transition from hypertensive heart disease to heart failure with preserved ejection fraction are poorly understood. When inappropriate for salt status, mineralocorticoid (deoxycorticosterone acetate) excess causes hypertrophy, fibrosis, and diastolic dysfunction. Because cardiac mineralocorticoid receptors are protected from mineralocorticoid binding by the absence of 11-beta hydroxysteroid dehydrogenase, salt-mineralocorticoid-induced inflammation is… CONTINUE READING
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