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Important pathophysiologic mechanisms in HF (1)

Important pathophysiologic mechanisms in HF (1). Important pathophysiologic mechanisms in HF (2). Important pathophysiologic mechanisms in HF (3). Neurohormonal model of HF.  -Blockade normalizes Ang II-provoked release of norepinephrine in HF. Molecular model of HF.

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Important pathophysiologic mechanisms in HF (1)

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  1. Important pathophysiologic mechanisms in HF (1)

  2. Important pathophysiologic mechanisms in HF (2)

  3. Important pathophysiologic mechanisms in HF (3)

  4. Neurohormonal model of HF

  5. -Blockade normalizes Ang II-provoked release of norepinephrine in HF

  6. Molecular model of HF

  7. Regulation of key molecules in cardiac EC coupling bystress-activated pathways

  8. Myocardial force generation increases in response to -blockade in HF after exposure to isoproterenol

  9. The RAAS in HF Angiotensinogen Kininogens Angiotensin I Bradykinin Nonspecific chymases ACE/kininase II • Bradykinin receptor • Norepinephrine • Vasodilation • Vessel permeability • tPA/prostaglandin release ACEinhibitors Angiotensin II Inactive peptides ARB • AT1 receptor • Myocardial fibrosis • Norepinephrine • Vasoconstriction • PAI/endothelin AT2 receptor  Myocardial fibrosis  Adrenal catechols ? Apoptosis  Sympatheticactivity  Nitric oxide Aldosterone Aldosteroneantagonists Improvedendothelial function Increased afterload disease progression The RAAS in HF RAAS = renin-angiotensin-aldosterone system Jamali AH et al. Arch Intern Med. 2001;161:667-72.

  10. Escape of Ang II despite ACE inhibition

  11. RESOLVD: Ang II concentrations similar at baseline and study end

  12. AT1-receptor blockade improves vasorelaxation in HF by upregulation of eNOS via AT2 receptors

  13. Primary targets of treatment in HF

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