Clues emerge about benefits of briefly blocking blood flow

Bjorn, Genevive

doi:10.1038/nm0209-132

Cited by 1 publication

(2 citation statements)

References 6 publications

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“…Nitroalkene derivatives of unsaturated fatty acids represent the convergence of such NO pathway with lipids4 since they are formed by NO and NO 2 − -dependent redox reactions1. Thus, they constitute a subset of molecules in the emerging physiological pool of the nitric oxide derived metabolome5, 6 that control the physiological homeostasis by coordinating adaptive responses7, 8. At present, the mechanisms underlying the production of nitrated lipids under biological conditions, specific structural isomer distributions, nitrated fatty acid-susceptible proteome and detailed biological signaling actions are incompletely characterized6.…”

Section: Introductionmentioning

confidence: 99%

“…For instance, nitro derivatives of linoleic and oleic (OA-NO 2 ) acids are activators of peroxisome proliferator-activated receptor-γ (PPARγ)14, 15, form covalent adducts with the p65 subunit of NF-κB16, and activate the Keap1/Nrf2 antioxidant response, reactions that promote adaptive responses in vascular cells17, 18. These derivatives of NO-mediated redox reactions represent an inflammatory-resolving adaptive response7. In the context of the vasculature, OA-NO 2 inhibits neointimal hyperplasia19 and exerts vasorelaxation of preconstricted aortic rings20.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nitro-Oleic Acid Inhibits Angiotensin II–Induced Hypertension

Zhang

Villacorta²,

Chang³

et al. 2010

Circulation Research

115

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Rationale: Nitro-oleic acid (OA-NO 2 ) is a bioactive, nitric-oxide derived fatty acid with physiologically relevant vasculoprotective properties in vivo. OA-NO 2 exerts cell signaling actions as a result of its strong electrophilic nature and mediates pleiotropic cell responses in the vasculature. Objective: The present study sought to investigate the protective role of OA-NO 2 in angiotensin (Ang) II–induced hypertension. Methods and Results: We show that systemic administration of OA-NO 2 results in a sustained reduction of Ang II–induced hypertension in mice and exerts a significant blood pressure lowering effect on preexisting hypertension established by Ang II infusion. OA-NO 2 significantly inhibits Ang II contractile response as compared to oleic acid (OA) in mesenteric vessels. The improved vasoconstriction is specific for the Ang II type 1 receptor (AT 1 R)-mediated signaling because vascular contraction by other G-protein–coupled receptors is not altered in response to OA-NO 2 treatment. From the mechanistic viewpoint, OA-NO 2 lowers Ang II–induced hypertension independently of peroxisome proliferation-activated receptor (PPAR)γ activation. Rather, OA-NO 2 , but not OA, specifically binds to the AT 1 R, reduces heterotrimeric G-protein coupling, and inhibits IP 3 (inositol-1,4,5-trisphosphate) and calcium mobilization, without inhibiting Ang II binding to the receptor. Conclusions: These results demonstrate that OA-NO 2 diminishes the pressor response to Ang II and inhibits AT 1 R-dependent vasoconstriction, revealing OA-NO 2 as a novel antagonist of Ang II–induced hypertension.

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