[Ca2+]i (cytosolic [Ca2+]) and OS (oxidative stress) were measured simultaneously in calf pulmonary artery endothelial cells using fura-2 and carboxy-2´,7´-dichlorodihydrofluorescein. ATP stimulated a [Ca2+]i increase that was followed a few seconds later by an increase in OS. Pre-exposure to 5 μM H2O2 potentiated these responses to ATP. Elevating or removing extracellular Ca2+ increased or reduced the [Ca2+]i response to ATP and caused parallel changes in the OS response, suggesting that this response was a consequence of the [Ca2+]i response. Inhibition of mitochondria with rotenone or antimycin A affected the responses but not in a manner that allowed a simple interpretation of the role of mitochondria. These data show an initimate connection between [Ca2+]i and OS that can be modulated by low levels of exogenously applied OS, allowing the possibility of positive feedback.

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