Figure 4.
Neuronal nitric oxide synthase (nNOS) compartmentation, function and mechanism in failing cardiac myocyte
nNOS protein expression and activity are increased in failing myocardium. nNOS translocates to plasma membrane and interacts with caveolin-3 (Cav3) but dissociates from ryanodine receptors (RyR). nNOS-derived NO changes the activities of Ca2+ handling proteins via S-nitrosylation. Cardiac-specific overexpression of nNOS is associated with increased nNOS localization in mitochondria and moderates mitochondria activity.