期刊
ACTA PHYSIOLOGICA
卷 222, 期 1, 页码 -出版社
WILEY
DOI: 10.1111/apha.12893
关键词
ageing; endothelial-dependent vasodilation; mitochondria-targeted antioxidant; MitoQ; nitric oxide bioavailability
类别
资金
- NIH Heart, Lung, Blood Institute [HL-091830]
- Veterans Affairs Rehabilitation Research and Development Merit [E6910-R]
- Medical Research Council [MC_UU_00015/3, MC_U105663142] Funding Source: researchfish
- MRC [MC_UU_00015/3, MC_U105663142] Funding Source: UKRI
AimThis study sought to determine the role of free radicals derived from mitochondria in the vasculature in the recognized age-related endothelial dysfunction of human skeletal muscle feed arteries (SMFAs). MethodsA total of 44 SMFAs were studied with and without acute exposure to the mitochondria-targeted antioxidant MitoQ and nitric oxide synthase (NOS) blockade. The relative abundance of proteins from the electron transport chain, phosphorylated (p-) to endothelial (e) NOS ratio, manganese superoxide dismutase (MnSOD) and the mitochondria-derived superoxide (O2-) levels were assessed in SMFA. Endothelium-dependent and endothelium-independent SMFA vasodilation was assessed in response to flow-induced shear stress, acetylcholine (ACh) and sodium nitroprusside (SNP). ResultsMitoQ restored endothelium-dependent vasodilation in the old to that of the young when stimulated by both flow (young: 68 5; old: 25 +/- 7; old + MitoQ 65 +/- 9%) and ACh (young: 97 +/- 4; old: 59 +/- 10; old + MitoQ: 98 +/- 5%), but did not alter the initially uncompromised, endothelium-independent vasodilation (SNP). Compared to the young, MitoQ in the old diminished the initially elevated mitochondria-derived
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