Lau K S, Grange R W, Chang W J, Kamm K E, Sarelius I, Stull J T
Department of Physiology, University of Texas Southwestern Medical Center at Dallas, 75235-9040, USA.
FEBS Lett. 1998 Jul 10;431(1):71-4. doi: 10.1016/s0014-5793(98)00728-5.
Nitric oxide generated by neuronal nitric oxide synthase in contracting skeletal muscle fibers may regulate vascular relaxation via a cGMP-mediated pathway. Neuronal nitric oxide synthase content is greatly reduced in skeletal muscles from mdx mice. cGMP formation increased in contracting extensor digitorum longus muscles in vitro from C57 control, but not mdx mice. The increase in cGMP content was abolished with NG-nitro-L-arginine. Sodium nitroprusside treatment increased cGMP levels in muscles from both C57 and mdx mice. Skeletal muscle contractions also inhibited phenylephrine-induced phosphorylation of smooth muscle myosin regulatory light chain. Arteriolar dilation was attenuated in contracting muscles from mdx but not C57 mice. NO generated in contracting skeletal muscle may contribute to vasodilation in response to exercise.
在收缩的骨骼肌纤维中，由神经元型一氧化氮合酶产生的一氧化氮可能通过环磷酸鸟苷（cGMP）介导的途径调节血管舒张。mdx小鼠骨骼肌中的神经元型一氧化氮合酶含量大幅降低。在体外，C57对照组的伸趾长肌收缩时cGMP生成增加，但mdx小鼠的则未增加。NG-硝基-L-精氨酸可消除cGMP含量的增加。硝普钠处理可提高C57和mdx小鼠肌肉中的cGMP水平。骨骼肌收缩还可抑制去氧肾上腺素诱导的平滑肌肌球蛋白调节轻链的磷酸化。mdx小鼠收缩肌肉中的小动脉扩张减弱，但C57小鼠的未减弱。收缩的骨骼肌中产生的一氧化氮可能有助于运动时的血管舒张。
