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Inotropic actions of adenosine derivatives in the mammalian heart
Author(s) -
Scholz H.,
Kohl C.,
Neumann J.,
Schmitz W.,
Seeland C.,
Stein B.
Publication year - 1993
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.430280315
Subject(s) - isoprenaline , contractility , medicine , endocrinology , adenosine , agonist , chemistry , cgs 21680 , phospholamban , contraction (grammar) , guinea pig , inositol , adenosine receptor , stimulation , receptor , calcium , biology
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. © 1993 Wiley‐Liss, Inc.