Premium
EFFECTS OF INTRACELLULAR Ca 2+ CHELATING ON NORADRENALINE RELEASE IN NORMOXIC AND ANOXIC HEARTS
Author(s) -
Du XiaoJun,
Bobik Alex,
Esler Murray D.,
Dart Anthony M.
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb02697.x
Subject(s) - anoxic waters , bapta , extracellular , intracellular , chemistry , chelation , biophysics , endogeny , biochemistry , biology , inorganic chemistry , environmental chemistry
SUMMARY 1. Ischaemia and anoxia induce excessive noradrenaline (NA) release in the heart by a mechanism independent of both nerve activity and extracellular Ca 2+ . The present study was designed to examine the potential role of intracellular Ca 2+ mobilization in anoxic NA release in the heart by chelating intracellular free Ca 2+ . 2. In normoxic hearts, preloading with an intracellular fre. Ca 2+ chelator (BAPTA) reduced neuronal NA release by 65%, confirming the effectiveness of the loading protocol. Release of NA independent of nerve activity occurred in hearts subjected to a 40 min period of anoxic, substrate‐free and nominal Ca 2+ ‐free perfusion. Loading hearts with BAPTA prior to anoxia failed to reduce NA overflow (1561 ± 147 vs 1496 ± 206 pmol/g over 40 min). Infusion with BAPTA (20 μmol/L) during the first 25 min of the anoxic period reduced the quantity of anoxic NA release by approximately 25% from 2013 ± 124 to 1476 ± 207 pmol/g ( P < 0.05). 3. Our results confirm that anoxic NA release is predominantly. Ca 2+ ‐independent process with Ca 2+ mobilization from endogenous storage playing only a minor contributing role.