Abstract
Background: Chronic phosphodiesterase type 5 inhibition (PDE5I) may enhance myocardial cGMP and restore cGMP dependent protein kinase (PKG) opposition to G-protein coupled receptor (GPCR) signaling in pressure overload (POL) induced heart failure (HF) and ameliorate maladaptive remodeling. However, if PKG signaling is not disrupted, PDE5I may not alter hypertrophic remodeling in POL states. Hypotheses: 1) Disruption of PKG signaling due to deletion of the natriuretic peptide receptor A (NPRA) is associated with exaggerated maladaptive remodeling in response to POL produced by transverse aortic constriction (TAC).
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