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PDE3 inhibition by C-type natriuretic peptide-induced cGMP enhances cAMP-mediated signaling in both non-failing and failing hearts

Eur. J. Pharmacol.. 2017-10; 
MeierSilja, AndressenKjetil Wessel, AronsenJan Magnus, SjaastadIvar, HougenKarina, SkomedalTor, OsnesJan-Bjørn, QvigstadEirik, LevyFinn Olav, MoltzauLise Ro
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Biochemicals … Cilostamide, rolipram, EHNA hydrochloride, CGP20712 dihydrochloride, ICI118551 hydrochloride were from Tocris Bioscience (Bristol, UK). BNP and CNP were from GenScript (Piscataway, NJ, US) and isoflurane (Forene) from Abbot Scandinavia (Solna, Sweden) … Get A Quote

摘要

We have previously shown that the natriuretic peptide receptor B (NPR-B) agonist C-type natriuretic peptide (CNP) enhances cyclic adenosine 3´,5´-monophosphate (cAMP)-mediated signaling in failing hearts, through cyclic guanosine 3´,5´-monophosphate (cGMP)-mediated phosphodiesterase (PDE) 3 inhibition. As several signaling pathways are importantly changed in failing hearts, it could not be taken for granted that this crosstalk would be the same in non-failing hearts. Thus, we wanted to clarify to which extent this effect of CNP occurred also in non-failing hearts. Inotropic and lusitropic responses were measured in muscle strips and cGMP levels, localized cAMP levels, cAMP-PDE activity and mRN... More

关键词

Guanylyl cyclase-A (GC-A),Guanylyl cyclase-B (GC-B),Heart failure,Inotropic response,Phosphodiesterase 3 (PDE3),β-adrenoce