Abstract
Background Atrial (ANP), B-type (BNP) and C-type (CNP) natriuretic peptide levels are increased in heart failure. Natriuretic peptides mediate their effects through natriuretic peptide receptors (NPRs), ANP and BNP preferentially through NPR-A and CNP through NPR-B. NPRs are membrane bound guanylyl cyclases that increase cyclic GMP (cGMP) production when activated. Increased cGMP levels may have beneficial cardiovascular effects through protein kinase G. In contrast, we have previously shown that NPR-B stimulation by CNP enhances b1-adrenoceptor (b1-AR) mediated signaling in failing hearts through inhibition of phosphodiesterase 3 (PDE3) [1]. This cardioexcitatory influence is longstanding and is thus probably detrimental in the failing heart. However, a comparison of the PDE3 inhibitory effect of NPR-B signaling in non-failing and failing hearts was not elucidated.
Highlights
Atrial (ANP), B-type (BNP) and C-type (CNP) natriuretic peptide levels are increased in heart failure. Natriuretic peptides mediate their effects through natriuretic peptide receptors (NPRs), ANP and BNP preferentially through NPR-A and CNP through NPR-B
We have previously shown that NPR-B stimulation by CNP enhances b1-adrenoceptor (b1-AR) mediated signaling in failing hearts through inhibition of phosphodiesterase 3 (PDE3) [1]
A comparison of the PDE3 inhibitory effect of NPR-B signaling in non-failing and failing hearts was not elucidated
Summary
Silja Meier1,2*, Jan Magnus Aronsen, Ivar Sjaastad, Finn Olav Levy, Tor Skomedal, Jan-Bjørn Osnes, Eirik Qvigstad. From 5th International Conference on cGMP: Generators, Effectors and Therapeutic Implications Halle, Germany. From 5th International Conference on cGMP: Generators, Effectors and Therapeutic Implications Halle, Germany. 24-26 June 2011
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