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cytoprotective effect of the NO-donor SNAP \nand its downstream cellular pathway. Mouse ESC-derived \ncardiomyocytes were subjected to 150-min simulated ischemia (SI) \nfollowed by 120-min reoxygenation or corresponding non-ischemic \nconditions. The following treatments were applied during SI or \nnormoxia: the NO-donor S-Nitroso-N-acetyl-D,L-penicillamine \n(SNAP), the protein kinase G (PKG) inhibitor, the KATP channel \nblocker glibenclamide, the particulate guanylate cyclase \nactivator brain type natriuretic peptide (BNP), and a non-\nspecific NO synthase inhibitor (N-Nitro-L-arginine, L-NNA) alone \nor in different combinations. Viability of cells was assayed by \npropidium iodide staining. SNAP attenuated SI-induced cell death \nin a concentration-dependent manner, and this protection was \nattenuated by inhibition of either PKG or KATP channels. \nHowever, SI-induced cell death was not affected by BNP or by L-\nNNA. We conclude that SNAP protects mESC-derived cardiomyocytes \nagainst SI/R injury and that soluble guanylate-cyclase, PKG, and \nKATP channels play a role in the downstream pathway of SNAP-\ninduced cytoprotection. 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