Abstract

We investigated the role of Ca2+ in generating reactive oxygen species (ROS) induced by hyposmotic stress (Hypo) and its relationship to regulatory volume decrease (RVD) in cardiomyocytes. Hypo-induced increases in cytoplasmic and mitochondrial Ca2+. Nifedipine (Nife) inhibited both Hypo-induced Ca2+ and ROS increases. Overexpression of catalase (CAT) induced RVD and a decrease in Hypo-induced blebs. Nife prevented CAT-dependent RVD activation. These results show a dual role of Hypo-induced Ca2+ influx in the control of cardiomyocyte viability. Hypo-induced an intracellular Ca2+ increase which activated RVD and inhibited necrotic blebbing thus favoring cell survival, while simultaneously increasing ROS generation, which in turn inhibited RVD and induced necrosis. © 2009 Federation of European Biochemical Societies.