To elucidate the mechanisms by which increased NO and decreased ROS may mediate protection against ischemia/reperfusion injury, we examined NO signaling via a GC-dependent pathway by measuring Ser239 phosphorylation and activation of the cGMP-dependent protein kinase (PKG) substrate vasodilator-stimulated protein (VASP) [55, 56]. Here, VASP is linked to ischemia.