From the Department of Pediatrics, Division of Pediatric Endocrinology and Diabetes (K.S.H.), Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute (K.S.H., S.G.W., M.D.-G., N.H., C.C., S.S., B.A.F., M.T.G.), Department of Pharmacology and Chemical Biology (S.G.W., M.D.-G., S.S., B.A.F.), Department of Medicine, Division of Endocrinology (N.H., B.G.), and Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, PA (M.T.G.); Department of Physics, Wake Forest University, Winston Salem, NC (L.B., D.B.K.-S.); and Pharmaceutical Development Section, Department of Pharmacy, Clinical Center, National Institutes of Health, Bethesda, MD (G.P., G.G.).
Hypertension. 2017 Sep;70(3):634-644. doi: 10.1161/HYPERTENSIONAHA.117.09016.
Dietary NO (nitrate) and NO (nitrite) support ˙NO (nitric oxide) generation and downstream vascular signaling responses. These nitrogen oxides also generate secondary nitrosating and nitrating species that react with low molecular weight thiols, heme centers, proteins, and unsaturated fatty acids. To explore the kinetics of NOand NOmetabolism and the impact of dietary lipid on nitrogen oxide metabolism and cardiovascular responses, the stable isotopes NaNO and NaNO were orally administered in the presence or absence of conjugated linoleic acid (cLA). The reduction of NO to NO was indicated by electron paramagnetic resonance spectroscopy detection of hyperfine splitting patterns reflecting NO-deoxyhemoglobin complexes. This formation of NO also translated to decreased systolic and mean arterial blood pressures and inhibition of platelet function. Upon concurrent administration of cLA, there was a significant increase in plasma cLA nitration products 9- and 12-NO-cLA. Coadministration of cLA with NO also impacted the pharmacokinetics and physiological effects of NO, with cLA administration suppressing plasma NOand NOlevels, decreasing NO-deoxyhemoglobin formation, NOinhibition of platelet activation, and the vasodilatory actions of NO, while enhancing the formation of 9- and 12-NO-cLA. These results indicate that the biochemical reactions and physiological responses to oral NOand NOare significantly impacted by dietary constituents, such as unsaturated lipids. This can explain the variable responses to NOand NOsupplementation in clinical trials and reveals dietary strategies for promoting the generation of pleiotropic nitrogen oxide-derived lipid signaling mediators. Clinical Trial Registration- URL: http://www.clinicaltrials.gov . Unique identifier: NCT01681836.
饮食中的硝酸盐(NO3-)和亚硝酸盐(NO2-)支持一氧化氮(NO)的生成和下游血管信号转导反应。这些氮氧化物还会生成次生的亚硝化和硝化物质,与低分子量硫醇、血红素中心、蛋白质和不饱和脂肪酸发生反应。为了探索 NO 和 NO 代谢的动力学以及饮食脂质对氮氧化物代谢和心血管反应的影响,在存在或不存在共轭亚油酸(cLA)的情况下口服给予稳定同位素 NaNO3 和 NaNO2。电子顺磁共振波谱检测到超精细分裂模式反映 NO-脱氧血红蛋白复合物的形成,表明 NO 还原为 NO。NO 的这种形成也导致收缩压和平均动脉压降低,血小板功能抑制。同时给予 cLA 时,血浆中 cLA 硝化产物 9-和 12-NO-cLA 显著增加。cLA 与 NO 同时给药也会影响 NO 的药代动力学和生理效应,cLA 给药会抑制血浆中 NO 和 NO 水平,减少 NO-脱氧血红蛋白的形成,NO 抑制血小板活化,以及 NO 的血管舒张作用,同时增强 9-和 12-NO-cLA 的形成。这些结果表明,饮食成分(如不饱和脂质)对口服 NO 和 NO 的生化反应和生理反应有显著影响。这可以解释临床试验中对 NO 和 NO 补充的反应差异,并揭示了促进多效性氮氧化物衍生的脂质信号介质生成的饮食策略。临床试验注册- URL:http://www.clinicaltrials.gov。唯一标识符:NCT01681836。