Kaasik A, Minajeva A, De Sousa E, Ventura-Clapier R, Veksler V
Laboratoire de Cardiologie Cellulaire et Moléculaire INSERM U-446, Université de Paris-Sud, Faculté de Pharmacie, Châtenay-Malabry, France.
FEBS Lett. 1999 Feb 5;444(1):75-7. doi: 10.1016/s0014-5793(99)00033-2.
Nitric oxide biosynthesis in cardiac muscle leads to a decreased oxygen consumption and lower ATP synthesis. It is suggested that this effect of nitric oxide is mainly due to the inhibition of the mitochondrial respiratory chain enzyme, cytochrome c oxidase. However, this work demonstrates that nitric oxide is able to inhibit soluble mitochondrial creatine kinase (CK), mitochondrial CK bound in purified mitochondria, CK in situ in skinned fibres as well as the functional activity of mitochondrial CK in situ in skinned fibres. Since mitochondrial isoenzyme is functionally coupled to oxidative phosphorylation, its inhibition also leads to decreased sensitivity of mitochondrial respiration to ADP and thus decreases ATP synthesis and oxygen consumption under physiological ADP concentrations.
心肌中一氧化氮的生物合成会导致耗氧量降低和ATP合成减少。有人认为一氧化氮的这种作用主要是由于对线粒体呼吸链酶细胞色素c氧化酶的抑制。然而，这项研究表明，一氧化氮能够抑制可溶性线粒体肌酸激酶（CK）、纯化线粒体中结合的线粒体CK、去皮纤维中原位的CK以及去皮纤维中原位线粒体CK的功能活性。由于线粒体同工酶在功能上与氧化磷酸化相偶联，其抑制也会导致线粒体呼吸对ADP的敏感性降低，从而在生理ADP浓度下降低ATP合成和耗氧量。
