This study was conducted to determine the effect of prolonged exposure to arachidonic-acid (506321) (AA) on electrically induced calcium transients in single neonatal rat ventricular myocytes and to clarify the part played by cyclo-oxygenase AA products in this effect. The role of free radicals in the AA induced effects on calcium dynamics was also considered. Cultured single ventricular myocytes isolated from 2 to 4 day old Sprague-Dawley-rats were used for electrically induced calcium transients. The effects of AA on calcium handling by the sarcolemma and the sarcoplasmic reticulum were measured by analyzing potassium-chloride induced depolarization, caffeine and ryanodine. Prostanoid formation and free radical formation were also monitored. Exposure to 10 to 30 micromolar AA caused a concentration dependent and reversible configuration change and eventually a cessation of calcium transients. Continued exposure caused a calcium overload. AA did not influence potassium induced calcium increase but did eliminate caffeine induced calcium transients. The formation of 6-oxo- prostaglandin-F1-alpha was influenced by AA in a concentration dependent manner, but thromboxane-B2 formation was not changed. Pretreatment with alpha-tocopherol significantly delayed times until cessation of calcium transients and calcium overload. The authors suggest that AA exposure cessation of electrically induced calcium transients and calcium overload may involve formation of free radicals.
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