Pertussis toxin unmasks stimulatory myocardial A 2-adenosine receptors on ventricular cardiomyocytes

Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A 1-adenosine receptor agonist (-)-N 6-phenylisopropyladenosine (R-PIA) in the presence of isoprénaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A 1-adenosine receptors are mediated via pertussis toxin-sensitive G-proteins. Furthermore, the decrease in contractile response by the A 1/A 2-adenosine receptor agonist 5′-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxic unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A 2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A 1-adenosine receptors, cAMP-increasing A 2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response.