Tan, T., Scholz, P.M. and Weiss, H.R. (2010) Hypoxia Inducible Factor-1 Improves the Negative Functional Effects of Natriuretic Peptide and Nitric Oxide Signaling in Hypertrophic Cardiac Myocytes. Life Sciences, 87, 9-16.
https://doi.org/10.1016/j.lfs.2010.05.002

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.