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Extracellular ATP induces Ca 2+ transients in cardiac myocytes which are potentiated by norepinephrine
Author(s) -
De Young Mary Beth,
Scarpa Antonio
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)80508-2
Subject(s) - extracellular , medicine , calcium , endocrinology , phentolamine , chemistry , propranolol , myocyte , receptor antagonist , norepinephrine , contractility , adrenergic receptor , intracellular , antagonist , receptor , biology , biochemistry , dopamine
Isolated rat ventricular cardiac myocytes loaded with the fluorescent calcium indicator fura2 showed significant changes in intracellular calcium concentrations upon exposure to > 1 μM ATP (EC 50 = 7.4 ± 1.3 μM, n = 4, SE), suggesting that extracellular ATP may have an important influence on myocardial contractility. The response was found to be highly ATP specific and required extracellular calcium. Furthermore, 30 s pretreatment of the cells with 0.2–1 μM norepinephrine decreased the concentration of ATP required for the Ca 2+ transient, shifting the EC 50 for ATP to 1.7 ± 0.1 μM ( n = 3, SE). β‐Propranolol (a β 1 ‐receptor antagonist) prevented potentiation, whereas phentolamine (an α 1 ‐receptor antagonist) did not, indicating that regulation is through the β 1 ‐adrenergic receptor. ATP and norepinephrine released locally from sympathetic neurons may act in concert through the ATP and β 1 ‐adrenergic receptors to regulate myocardial calcium homeostasis.