Adenylyl cyclase-dependent inhibition of myocardial norepinephrine release by presynaptic adenosine A1-receptors

Christof Burgdorf*, Frank Schütte, Thomas Kurz, Andreas Dendorfer, Gert Richardt

*Corresponding author for this work
4 Citations (Scopus)


Adenosine A1-receptor-mediated inhibition of exocytotic norepinephrine (NE) release from sympathetic nerve endings has been implicated as an endogenous cardioprotective mechanism. So far, the intraneuronal signal transduction underlying the adenosine A1-receptor-elicited inhibition of NE release is not known. In the present study, we determined in isolated Langendorff-perfused rat hearts the role of inhibitory G-proteins and of adenylyl cyclase (AC) on NE release after pharmacologic adenosine A 1-receptor activation. NE release was induced by electrical field stimulation and was assessed in the coronary effluent by high-performance liquid chromatography. Adenosine A1-receptor activation with 2-chloro-N6-cyclopentyladenosine (CCPA) decreased NE release by ∼50% in hearts from both untreated and pertussis toxin-pretreated rats. In hearts from untreated rats, suppression of NE release in response to CCPA was completely abolished by the cell-permeable AC inhibitor 9-(tetrahydro-2′- furyl)adenine (SQ 22536). Direct activation of AC with forskolin increased NE release by ∼20%. In the presence of forskolin, stimulation of adenosine A1-receptors with CCPA or inhibition of AC with SQ 22536 decreased NE release to baseline. These findings suggest a Gi-protein-independent but AC-dependent inhibition of NE release following adenosine A 1-receptor activation.

Original languageEnglish
JournalJournal of Cardiovascular Pharmacology
Issue number1
Pages (from-to)1-3
Number of pages3
Publication statusPublished - 01.01.2005

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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