摘要

It is now clear that both endogenous and exogenous sources of nitric oxide(NO) exert important modulatory effects on cardiac mitochondrial function.There is also growing evidence that NO can be produced within the mitochondria themselves.NO can influence respiratory activity,both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation.At pathological concentrations,NO causes irreversible alterations in respiratory function and also interacts with reactive oxygen species(ROS) to form reactive nitrogen species(RNS),which may further impair mitochondrial respiration and even lead to open the mitochondrial permeability transition pore and induce cell death.Diabetes,aging,myocardial ischemia,and heart failure are all associated with altered ROS generation,which can alter the delicate regulatory balance of effects of NO in the mitochondria.