Key result
PDE5A inhibition by EMD82639 blunted dobutamine-enhanced function in normal dogs but had negligible effects in failing hearts, which had 50% lower PDE5A protein expression.
Why the study?
Does PDE5A inhibition modulate beta-adrenergic signaling differently in normal versus failing hearts?
Population
Normal conscious dogs and dogs with heart failure (tachypacing model)
Comparison
PDE5A inhibition by EMD82639 vs Normal vs failing hearts; basal vs…
Design
Preclinical
Authors
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PDE5A inhibition may not enhance beta-adrenergic function in failing hearts; leaves open relevance to human HF pending further study.
Does PDE5A inhibition modulate beta-adrenergic signaling differently in normal versus failing hearts?
PDE5A modulates beta-adrenergic stimulation in the normal heart, but its down-regulation and altered localization in heart failure may contribute to blunted beta-adrenergic responsiveness.
Senzaki et al. (2001) studied Heart failure. EMD82639 vs. Normal dogs was evaluated on Systolic and diastolic function and PDE5A protein expression. PDE5A inhibition by EMD82639 blunted dobutamine-enhanced function in normal dogs but had negligible effects in failing hearts, which had 50% lower PDE5A protein expression.
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