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- W2890182510 endingPage "926" @default.
- W2890182510 startingPage "914" @default.
- W2890182510 abstract "Neuronal nitric oxide synthase (nNOS) is involved in nitric oxide (NO) production and suggested to play a crucial role in blood flow regulation of skeletal muscle. During activation of the muscle, NO helps attenuate the sympathetic vasoconstriction to accommodate increased metabolic demands, a phenomenon known as functional sympatholysis. In inherited myopathies such as the dystrophinopathies Duchenne and Becker muscle dystrophies (DMD and BMD), nNOS is lost from the sarcolemma. The loss of nNOS may cause functional ischemia contributing to skeletal and cardiac muscle cell injury. Effects of NO is augmented by inhibiting degradation of the second messenger cyclic guanosine monophosphate (cGMP) using sildenafil and tadalafil, both of which inhibit the enzyme phosphodiesterase 5 (PDE5). In animal models of DMD, PDE5-inhibitors prevent functional ischemia, reduce post-exercise skeletal muscle pathology and fatigue, show amelioration of cardiac muscle cell damage and increase cardiac performance. However, effect on clinical outcomes in DMD and BMD patients have been disappointing with minor effects on upper limb performance and none on ambulation. This review aims to summarize the current knowledge of nNOS function related to functional sympatholysis in skeletal muscle and studies on PDE5-inhibitor treatment in nNOS-deficient animal models and patients." @default.
- W2890182510 created "2018-09-27" @default.
- W2890182510 creator A5019029992 @default.
- W2890182510 creator A5023543224 @default.
- W2890182510 creator A5045989095 @default.
- W2890182510 creator A5049640728 @default.
- W2890182510 date "2018-11-01" @default.
- W2890182510 modified "2023-10-16" @default.
- W2890182510 title "Role of neuronal nitric oxide synthase (nNOS) in Duchenne and Becker muscular dystrophies – Still a possible treatment modality?" @default.
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