Hopkins, W.E., Chen, Z., Fukagawa, N.K., Hall, C., Knot, H.J. and LeWinter, M.M. (2004) Increased Atrial and Brain Natriuretic Peptides in Adults with Cyanotic Congenital Heart Disease: Enhanced Understanding of the Relationship between Hypoxia and Natriuetic Peptide Secretion. Circulation, 109, 2872-2877.
https://doi.org/10.1161/01.CIR.0000129305.25115.80

has been cited by the following article:

• TITLE: Forskolin Modulates the Inhibitory Effect of C-Type Natriuretic Peptide on Hypoxia-Induced Atrial Dynamics and Hypoxia Inducible Factor 1 Alpha Activity

  AUTHORS: Chengming Guan, Yanan Jia, Chaochao Bian, Bo Zhang, Dazhi Ding, Xun Cui

  KEYWORDS: C-Type Natriuretic Peptide, Hypoxia Inducible Factor-1α, Phosphodiesterase, Adenylyl Cyclase, Forskolin

  JOURNAL NAME: Journal of Biosciences and Medicines, Vol.5 No.1, January 3, 2017

  ABSTRACT: Our study investigated effects of C-type natriuretic peptide (CNP) on atrial dynamics and hypoxia inducible factor 1 alpha (HIF-1α) activity in perfused beating rat atria, under hypoxic conditions. Hypoxia significantly increased the levels of HIF-1α, concomitant with decreased trial dynamics. CNP (0.1 μmol/L) further decreased atrial dynamics under hypoxia and suppressed hypoxia-induced stimulation of HIF-1α expression. An adenylylcyclase (AC) activator, forskolin (0.1 μmol/L), significantly up-regulated atrial phosphodiesterase subtype 3A (PDE 3A) protein without affecting hypoxia-induced dynamics. In the presence of forskolin, the inhibitory effects of CNP on hypoxia-induced atrial dynamics and HIF-1α levels were significantly attenuated. Forskolin also prevented hypoxia-induced downregulation of PDE3A protein. These findings suggested that CNP inhibited atrial dynamics and HIF-1α activity in the isolated perfused beating rat atria under hypoxic conditions. Furthermore, both effects were modulated by the AC activator forskolin, through activation of CNP-PDE 3A signaling.