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EFFECTS of the calmodulin inhibitor calmidazolium on stimulation of nitric oxide (NO) release were investigated in neuroblastoma N1E-115 cells. NO release was determined indirectly by measuring cyclic GMP formation. Instead of the expected decrease in NO generation based on the calmodulin dependence of neuronal NO synthase, calmidazoline paradoxically increased cyclic GMP formation. Maximal activation occurred at 3 min and the effects were concentration dependent. This calmidazolium-stimulated NO release was markedly blocked by hemoglobin and N-monomethyl-L-arginine.