Abstract:
:We report a novel action of intracellular adenosine monophosphate (AMP) to inhibit beta-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 beta-adrenergic signaling by directly inhibiting PKA activity, independently of A(1)-purinergic receptor.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Ogura K,Miake J,Sasaki N,Iwai C,Bahrudin U,Li P,Kato M,Iitsuka K,Hirota Y,Koshida T,Yamamoto Y,Inoue Y,Yano A,Adachi M,Igawa O,Kurata Y,Morisaki T,Shiota G,Shirayoshi Y,Haruaki N,Hisatome Idoi
10.1016/j.yjmcc.2007.07.059subject
Has Abstractpub_date
2007-11-01 00:00:00pages
648-52issue
5eissn
0022-2828issn
1095-8584pii
S0022-2828(07)01168-6journal_volume
43pub_type
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