Stein B, Mende U, Neumann J, Schmitz W, Scholz H
Abteilung Allgemeine Pharmakologie, Universitäts-Krankenhaus Eppendorf, Hamburg, Germany.
J Mol Cell Cardiol. 1993 Jun;25(6):655-9. doi: 10.1006/jmcc.1993.1078.
Pertussis toxin-pretreatment abolished the contractility- and cAMP-decreasing effects of the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (R-PIA) in the presence of isoprenaline in isolated ventricular cardiomyocytes from guinea-pigs, indicating that these stimulatory effects of A1-adenosine receptors are mediated via pertussis toxin-sensitive G-proteins. Furthermore, the decrease in contractile response by the A1/A2-adenosine receptor agonist 5'-N-ethylcarboxamidadenosine (NECA) was abolished. Moreover, NECA increased cAMP content in pertussis toxin-pretreated cells. Thus, pertussis toxin unmasked cAMP-augmenting effects of NECA, indicating that NECA can stimulate A2-adenosine receptors on cardiomyocytes. Thereby, the present study provides evidence that besides cAMP- and contractility-decreasing A1-adenosine receptors, cAMP-increasing A2-adenosine receptors coexist on ventricular cardiomyocytes, which do not influence contractile response.
百日咳毒素预处理消除了豚鼠离体心室心肌细胞中，在异丙肾上腺素存在的情况下，A1-腺苷受体激动剂（-）-N6-苯基异丙基腺苷（R-PIA）的收缩性和cAMP降低作用，表明A1-腺苷受体的这些刺激作用是通过百日咳毒素敏感的G蛋白介导的。此外，A1/A2-腺苷受体激动剂5'-N-乙基羧酰胺腺苷（NECA）引起的收缩反应降低也被消除。此外，NECA增加了百日咳毒素预处理细胞中的cAMP含量。因此，百日咳毒素揭示了NECA的cAMP增强作用，表明NECA可以刺激心肌细胞上的A2-腺苷受体。从而，本研究提供了证据，除了降低cAMP和收缩性的A1-腺苷受体外，增加cAMP的A2-腺苷受体也共存于心室心肌细胞上，它们不影响收缩反应。
