Cross-talk Between Nitrate-Nitrite-NO and NO Synthase Pathways in Control of Vascular NO Homeostasis

Carlström, M; Liu, M; Yang, T; Zollbrecht, C; Huang, L; Peleli, M; Borniquel, S; Kishikawa, H; Hezel, M; Persson, AE; Weitzberg, E; Lundberg, JO

HERO ID

2232708

Reference Type

Journal Article

Year

2014

Language

English

PMID

24224525

HERO ID 2232708
In Press No
Year 2014
Title Cross-talk Between Nitrate-Nitrite-NO and NO Synthase Pathways in Control of Vascular NO Homeostasis
Authors Carlström, M; Liu, M; Yang, T; Zollbrecht, C; Huang, L; Peleli, M; Borniquel, S; Kishikawa, H; Hezel, M; Persson, AE; Weitzberg, E; Lundberg, JO
Journal Antioxidants & Redox Signaling
Volume 23
Issue 4
Page Numbers 295-306
Abstract Abstract 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 1 mmol 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. 00, 000-000.
Doi 10.1089/ars.2013.5481
Pmid 24224525
Wosid WOS:000363895200002
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English