Inhibition of β-adrenergic signaling by intracellular AMP is independent of cell-surface adenosine receptors in rat cardiac cells
| Autor: | Chisato Iwai, Osamu Igawa, Toshiya Koshida, Takayuki Morisaki, Kazuyoshi Ogura, Goshi Shiota, Akio Yano, Yasutaka Yamamoto, Ichiro Hisatome, Yoshiaki Inoue, Udin Bahrudin, Kazuhiko Iitsuka, Yasuaki Shirayoshi, Masamitsu Adachi, Yasutaka Kurata, Yutaka Hirota, Junichiro Miake, Masaru Kato, Norihito Sasaki, Peili Li, Ninomiya Haruaki |
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| Rok vydání: | 2007 |
| Předmět: |
Adenosine monophosphate
Adenosine Heart Ventricles Action Potentials Pharmacology Biology chemistry.chemical_compound Adenosine A1 receptor Receptors Adrenergic beta medicine Animals Ventricular Function Rats Wistar Molecular Biology Cell Membrane Receptors Purinergic P1 Heart Purinergic signalling Adenosine A3 receptor Adenosine receptor Adenosine Monophosphate Rats chemistry Cardiology and Cardiovascular Medicine Adenosine A2B receptor Intracellular Signal Transduction medicine.drug |
| Zdroj: | Journal of Molecular and Cellular Cardiology. 43:648-652 |
| ISSN: | 0022-2828 |
| Popis: | We report a novel action of intracellular adenosine monophosphate (AMP) to inhibit β-adrenergic signaling in isolated rat ventricular myocytes. Extracellular application of adenosine or AMP suppressed isoproterenol (Iso)-induced prolongation of action potential duration (APD). This effect was completely abolished by an A 1 -receptor antagonist, DPCPX. Intracellular application of AMP, but not adenosine, attenuated Iso-induced APD prolongation. Iso-induced increases in the L-type Ca 2+ current (I Ca,L ) were also inhibited by intracellular AMP. These inhibitory effects were not affected by either DPCPX or glibenclamide. In vitro, AMP directly inhibited PKA activity via binding to its regulatory subunit. These results suggest that intracellular AMP attenuates β-adrenergic signaling by directly inhibiting PKA activity, independently of A 1 -purinergic receptor. |
| Databáze: | OpenAIRE |
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