期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 23, 期 4, 页码 295-306出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2013.5481
关键词
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资金
- Swedish Research Council [K2012-99X-21971-01-3]
- Vinnova (CIDaT)
- Swedish Heart and Lung Foundation [20110589]
- Jeanssons Foundation [JS2011-0212]
- Torsten Soderbergs Foundation
- EUs 7th Framework program (Flaviola)
- Wenner-Gren Foundation
- Swedish Society for Medical Research (SSMF)
Aims: Inorganic nitrate and nitrite from endogenous and dietary sources have emerged as alternative substrates for nitric oxide (NO) formation in addition to the classic L-arginine NO synthase (NOS)-dependent pathway. Here, we investigated a potential cross-talk between these two pathways in the regulation of vascular function. Results: Long-term dietary supplementation with sodium nitrate (0.1 and 1mmol kg(-1) day(-1)) in rats caused a reversible dose-dependent reduction in phosphorylated endothelial NOS (eNOS) (Ser1177) in aorta and a concomitant increase in phosphorylation at Thr495. Moreover, eNOS-dependent vascular responses were attenuated in vessels harvested from nitrate-treated mice or when nitrite was acutely added to control vessels. The citrulline-to-arginine ratio in plasma, as a measure of eNOS activity, was reduced in nitrate-treated rodents. Telemetry measurements revealed that a low dietary nitrate dose reduced blood pressure, whereas a higher dose was associated with a paradoxical elevation. Finally, plasma cyclic guanosine monophosphate increased in mice that were treated with a low dietary nitrate dose and decreased with a higher dose. Innovation and Conclusions: These results demonstrate the existence of a cross-talk between the nitrate-nitrite-NO pathway and the NOS-dependent pathway in control of vascular NO homeostasis. Antioxid. Redox Signal. 23, 295-306.
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