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Exogenous ATP regulates excitation‐induced force in isolated muscle through the P2Y receptor family
Author(s) -
BrochLips Martin,
Pedersen Thomas Holm,
Nielsen Ole Bækgaard
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.962.8
Subject(s) - p2y receptor , receptor , purinergic receptor , chemistry , phospholipase c , extracellular , skeletal muscle , medicine , endocrinology , contractility , agonist , p2 receptor , ionotropic effect , ppads , biophysics , biology , biochemistry , nmda receptor
In skeletal muscles, contractions elicit a release of ATP into the extracellular space. Extracellular ATP has been recognized as an autocrine and paracrine signaling molecule acting on two purinergic receptor families; the metabotrophic P2Y receptors and the ionotropic P2X receptors. In this study we investigate the role of P2 receptors on the excitability and contractility of isolated skeletal muscle. Tetanic force production and M‐wave amplitude and area were investigated in isolated rat soleus muscles incubated in Krebs‐Ringer buffer. Exogenously added P2‐receptor agonist (ATP) and phospholipase C (PLC) inhibitor (U73122) were used to investigate P2‐receptor mediated effects on muscle function under conditions with compromised muscle excitability. When the excitability of muscles was depressed by elevating [K + ] o to 10 mM, tetanic force was reduced to 24 ± 2 % of initial force at 4 mM K + . However, upon addition of 1 mM ATP, force was recovered to 65 ± 8 % of initial force at 4 mM K + ( P < 0.001, n = 5). The force recovery was accompanied by a recovery of M‐wave area and amplitude from 20 ± 5 to 81 ± 11 % ( P < 0.05) and 8 ± 1 to 47 ± 11 % ( P < 0.05) of initial M‐wave area and amplitude at 4 mM K + , respectively ( n = 4). ATP induced force recovery could be eliminated by 50 μM PLC inhibitor indicating that the force recovery was mediated by the P2Y receptor family. Danish Medical Research Council (j. nr. 271‐05‐0304)