From the Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA (M.A.O., A.M.R., J.R.M., N.K., S.H., A.A.Q.); and Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, GA (J.L., A.M.).
Arterioscler Thromb Vasc Biol. 2014 Jun;34(6):1320-7. doi: 10.1161/ATVBAHA.113.303136. Epub 2014 Mar 27.
Abnormalities in nitric oxide (NO) bioavailability have been reported in blacks. Whether there are differences in endothelium-derived hyperpolarizing factor (EDHF) in addition to NO between blacks and whites and how these affect physiological vasodilation remain unknown. We hypothesized that the bioavailability of vascular NO and EDHF, at rest and with pharmacological and physiological vasodilation, varies between whites and blacks.
In 74 white and 86 black subjects without known cardiovascular disease risk factors, forearm blood flow was measured using plethysmography at rest and during inhibition of NO with N(G)-monomethyl-L-arginine and of K(+) Ca channels (EDHF) with tetraethylammonium. The reduction in resting forearm blood flow was greater with N(G)-monomethyl-L-arginine (P=0.019) and similar with tetraethylammonium in whites compared with blacks. Vasodilation with bradykinin, acetylcholine, and sodium nitroprusside was lower in blacks compared with whites (all P<0.0001). Inhibition with N(G)-monomethyl-L-arginine was greater in whites compared with blacks with bradykinin, acetylcholine, and exercise. Inhibition with tetraethylammonium was lower in blacks with bradykinin, but greater during exercise and with acetylcholine.
The contribution to both resting and stimulus-mediated vasodilator tone of NO is greater in whites compared with blacks. EDHF partly compensates for the reduced NO release in exercise and acetylcholine-mediated vasodilation in blacks. Preserved EDHF but reduced NO bioavailability and sensitivity characterizes the vasculature in healthy blacks.
http://clinicaltrials.gov/. Unique identifier: NCT00166166.
已有报道称,一氧化氮(NO)生物利用度异常存在于黑人中。除了 NO 之外,黑人与白人之间内皮衍生超极化因子(EDHF)是否存在差异,以及这些差异如何影响生理血管舒张仍不清楚。我们假设,血管 NO 和 EDHF 的生物利用度在休息时以及通过药理学和生理血管舒张,在白人和黑人之间存在差异。
在 74 名白人受试者和 86 名黑人受试者中,这些受试者没有已知的心血管疾病危险因素,使用容积描记法测量休息时和使用 N(G)-单甲基-L-精氨酸抑制 NO 以及四乙铵抑制 K(+)Ca 通道(EDHF)时的前臂血流量。与黑人相比,白人中 N(G)-单甲基-L-精氨酸(P=0.019)和四乙铵引起的休息时前臂血流减少更大。与白人相比,黑人的缓激肽、乙酰胆碱和硝普钠引起的血管舒张作用更低(均 P<0.0001)。与黑人相比,用缓激肽、乙酰胆碱和运动抑制 N(G)-单甲基-L-精氨酸时,白人的抑制作用更大。用缓激肽抑制四乙铵时,黑人的抑制作用较低,但运动时和用乙酰胆碱时抑制作用较大。
与黑人相比,NO 对休息时和刺激介导的血管舒张的贡献在白人中更大。EDHF 部分补偿了黑人运动和乙酰胆碱介导的血管舒张时 NO 释放减少。在健康的黑人中,血管特征为 EDHF 保持不变,但 NO 生物利用度和敏感性降低。