Key result
Stimulation of NPR-B by C-type natriuretic peptide enhanced beta1-adrenoceptor-evoked contractile responses and promoted cardiomyocyte apoptosis through cGMP-mediated inhibition of PDE3.
Why the study?
Does C-type natriuretic peptide enhance beta1-adrenoceptor signalling and promote apoptosis in failing hearts?
Population
Male Wistar rats with heart failure induced by coronary artery ligation
Comparison
C-type natriuretic peptide / NPR-B stimulation vs Selective PDE3 inhibitor cilostamide
Design
Preclinical
Authors
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Cautions against assuming net benefit from CNP in HF; leaves open whether NPR-B stimulation promotes apoptosis in patients.
Does C-type natriuretic peptide enhance beta1-adrenoceptor signalling and promote apoptosis in failing hearts?
CNP enhances beta1-adrenergic signaling and promotes apoptosis in failing hearts via PDE3 inhibition, suggesting a potentially detrimental long-term effect similar to chronic beta-adrenergic stimulation.
Qvigstad et al. (2009) studied Heart failure. C-type natriuretic peptide (CNP) was evaluated on beta1-adrenoceptor-evoked contractile responses and cardiomyocyte apoptosis. Stimulation of NPR-B by C-type natriuretic peptide enhanced beta1-adrenoceptor-evoked contractile responses and promoted cardiomyocyte apoptosis through cGMP-mediated inhibition of PDE3.
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