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一氧化氮对老年人渐进性握力运动中肱动脉血管舒张的贡献。

Contribution of nitric oxide to brachial artery vasodilation during progressive handgrip exercise in the elderly.

机构信息

Geriatric Research, Education, and Clinical Center, George E. Whalen VA Medical Center, Salt Lake City, Utah;

出版信息

Am J Physiol Regul Integr Comp Physiol. 2013 Oct 15;305(8):R893-9. doi: 10.1152/ajpregu.00311.2013. Epub 2013 Aug 15.

DOI:10.1152/ajpregu.00311.2013
PMID:23948773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3798772/
Abstract

UNLABELLED

The reduction in nitric oxide (NO)-mediated vascular function with age has largely been determined by flow-mediated dilation (FMD). However, in light of recent uncertainty surrounding the NO dependency of FMD and the recognition that brachial artery (BA) vasodilation during handgrip exercise is predominantly NO-mediated in the young, we sought to determine the contribution of NO to BA vasodilation in the elderly using the handgrip paradigm. BA vasodilation during progressive dynamic (1 Hz) handgrip exercise performed at 3, 6, 9, and 12 kg was assessed with and without NO synthase (NOS) inhibition [intra-arterial N(G)-monomethyl-l-arginine (l-NMMA)] in seven healthy older subjects (69 ± 2 yr). Handgrip exercise in the control condition evoked significant BA vasodilation at 6 (4.7 ± 1.4%), 9 (6.5 ± 2.2%), and 12 kg (9.5 ± 2.7%). NOS inhibition attenuated BA vasodilation, as the first measurable increase in BA diameter did not occur until 9 kg (4.0 ± 1.8%), and the change in BA diameter at 12 kg was reduced by ∼30% (5.1 ± 2.2%), with unaltered shear rate (

CONTROL

407 ± 57, l-NMMA: 427 ± 67 s(-1)). Although shifted downward, the slope of the relationship between BA diameter and shear rate during handgrip exercise was unchanged (

CONTROL

0.0013 ± 0.0004, l-NMMA: 0.0011 ± 0.007, P = 0.6) as a consequence of NOS inhibition. Thus, progressive handgrip exercise in the elderly evokes a robust BA vasodilation, the magnitude of which was only minimally attenuated following NOS inhibition. This modest contribution of NO to BA vasodilation in the elderly supports the use of the handgrip exercise paradigm to assess NO-dependent vasodilation across the life span.

摘要

目的

在老年人中,使用握力范式来确定一氧化氮(NO)对肱动脉(BA)血管舒张的贡献。

方法和结果

在 7 名健康老年人(69 ± 2 岁)中,在 3、6、9 和 12 kg 时进行逐渐动态(1 Hz)握力运动期间,评估有无一氧化氮合酶(NOS)抑制(动脉内 N(G)-单甲基-L-精氨酸(l-NMMA))的情况下,BA 血管舒张。在对照条件下,握力运动引起 BA 显著舒张,在 6(4.7 ± 1.4%)、9(6.5 ± 2.2%)和 12 kg(9.5 ± 2.7%)时。NOS 抑制减弱了 BA 血管舒张,因为第一次可测量的 BA 直径增加直到 9 kg 才发生(4.0 ± 1.8%),并且 12 kg 时 BA 直径的变化减少了约 30%(5.1 ± 2.2%),而剪切率未改变(

对照

407 ± 57,l-NMMA:427 ± 67 s(-1))。尽管向下移位,但握力运动期间 BA 直径与剪切率之间的关系斜率保持不变(

对照

0.0013 ± 0.0004,l-NMMA:0.0011 ± 0.007,P = 0.6),因为 NOS 抑制。因此,老年人的渐进性握力运动引起了强烈的 BA 血管舒张,在 NOS 抑制后,其幅度仅略有减弱。老年人 BA 血管舒张中 NO 的这种适度贡献支持使用握力运动范式来评估整个生命周期中依赖于 NO 的血管舒张。

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