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Cardiovascular Research 1995 30(6):889-898; doi:10.1016/S0008-6363(95)00133-6
© 1995 by European Society of Cardiology
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Copyright © 1995, European Society of Cardiology

Arachidonic acid disrupts calcium dynamics in neonatal rat cardiac myocytes

Peter Hoffmannb, Donald Richardsa, Ingrid Heinroth-Hoffmannc, Patty Mathiasa, Howard Weya and Mark Toraason*

aCenters for Disease Control and Prevention, National Institute for Occupational Safety and Health, Cellular Toxicology Section, Cincinnati, OH 45226, USA
bSanofi Research, 195 Route d'Espagne, B.P. 1169, 31036 Toulouse Cedex, France
cInstitute of Pharmacology and Toxicology, Martin Luther University, Halle, Germany

* Corresponding author.

Objectives: The purpose of this study was to investigate the effects of prolonged arachidonic acid (AA) exposure on electrically induced fluctuations of cytosolic free Ca2+ concentration ([Ca2+]i) in cardiac myocytes and to identify intracellular biochemical events that may play a role in the actions of AA on [Ca2+]i dynamics. Methods: Electrically induced [Ca2+]i transients were investigated in cultured single neonatal rat ventricular myocytes using spectrofluorometric analysis of fura-2-[Ca2+]i binding. KCl-induced depolarization, caffeine and ryanodine were used to assess the effects of AA on Ca2+ handling by the sarcolemma and the sarcoplasmic reticulum. Prostanoid formation was measured with an ELISA technique. {alpha}-Tocopherol was used to determine if free radical formation was a factor in the AA effects on [Ca2+]i. Results: Exposure to 10–30 µM AA produced a concentration-dependent and reversible configuration change and eventually a cessation of [Ca2+]i transients. Continued exposure resulted in a Ca2+ overload (tonic [Ca2+]i greater than peak systolic [Ca2+]i). AA did not influence KCl-induced [Ca2+]i increase but did eliminate caffeine-induced [Ca2+]i transients. AA exposure stimulated the formation of 6-oxo-prostaglandin F1{alpha} in a concentration-dependent manner, but thromboxane B2 formation was not influenced. {alpha}-Tocopherol pretreatment significantly delayed times till cessation of [Ca2+]i transients and Ca2+ overload, whereas ryanodine and cyclo-oxygenase inhibitors were without effect. Conclusions: The present data provide evidence that the initial action of AA on [Ca2+]i transients during excitation-contraction coupling involves an effect of AA on sarcolemmal Ca2+ influx and sarcoplasmic reticulum Ca2+ handling. AA-induced cessation of electrically induced [Ca2+]i transients and Ca2+ overload may involve the formation of free radicals.

KEYWORDS Arachidonic acid; Calcium; intracellular concentration; Calcium transients; Calcium overload; SR; SR; calcium release; Rat; ventricular myocytes


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