Adenosine receptor stimulation modulates contractility and intracellular signaling pathways in guinea-pig ventricular cardiomyocytes, with differential effects depending on the specific receptor subtype and presence of isoprenaline.
Animal cardiomyocyte data extend adenosine receptor signaling insights; leaves open human cardiac relevance.
The effects of adenosine receptor (AR) stimulation on contractile parameters as well as inositol phosphates, cAMP content, and phospholamban‐phosphorylation was studied in cardiac preparations. In guinea‐pig papillary muscles adenosine increased inositol trisphosphate formation and also slightly elevated force of contraction. In the presence of isoprenaline, however, adenosine still enhanced inositol trisphosphate formation but reduced force of contraction. In isolated electrically driven guinea‐pig ventricular cardiomyocytes the A 1 ‐AR agonist R‐PIA and the A 1 /A 2 ‐AR agonist NECA reduced isoprenaline‐stimulated contractility but only R‐PIA decreased isoprenaline‐enhanced cAMP content. The selective A 2 ‐AR agonist CGS 21680 increased isoprenaline‐stimulated cAMP content. This effect of CGS 21680 was antagonized by the A 2 ‐AR antagonist CGS 15943A and was increased after pertussis toxin‐pretreatment. Furthermore, R‐PIA and NECA decreased via A 1 ‐ARs the isoprenaline‐stimulated phospholamban‐phosphorylation in guinea‐pig ventricular cardiomyocytes.
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Scholz et al. (1993) studied this question.
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