Effects of intracellular Ca2+ chelating on noradrenaline release in normoxic and anoxic hearts.

Abstract

1. Ischaemia and anoxia induce excessive noradrenaline (NA) release in the heart by a mechanism independent of both nerve activity and extracellular Ca2+. The present study was designed to examine the potential role of intracellular Ca2+ mobilization in anoxic NA release in the heart by chelating intracellular free Ca2+. 2. In normoxic hearts, preloading with an intracellular free Ca2+ 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 mumol/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 a Ca(2+)-independent process with Ca2+ mobilization from endogenous storage playing only a minor contributing role.

• Authors: X J Du, A Bobik, M D Esler, A M Dart
• Journal: Clinical and experimental pharmacology & physiology (Clin Exp Pharmacol Physiol) Vol. 24 Issue 11 Pg. 819-23 (Nov 1997) ISSN: 0305-1870 [Print] Australia
• PMID: 9363363 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Chelating Agents
• Egtazic Acid
• 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid
• Oxygen
• Calcium
• Norepinephrine

Topics

• Animals
• Calcium (chemistry, metabolism)
• Chelating Agents (chemistry)
• Egtazic Acid (analogs & derivatives, chemistry)
• Electric Stimulation
• Heart (innervation)
• Hypoxia (metabolism)
• Male
• Myocardium (metabolism)
• Norepinephrine (metabolism)
• Oxygen (metabolism)
• Rats
• Rats, Sprague-Dawley