Maria F. Garcia-Saura

TL;DR: In this article, it was shown that nitrite is remarkably efficient at modifying the same protein sites, and that physiological nitrite concentrations account for the basal levels of these modifications in vivo.

TL;DR: Most tissues (except erythrocytes) produce free NO at rates that are maximal under hypoxia and that correlate robustly with each tissue's capacity for mitochondrial oxygen consumption, as well as comparing the kinetics of NO release before and after ferricyanide addition in tissue homogenates to mathematical models of \batchmode.

TL;DR: Breathing Nitric oxide leads to the rapid accumulation of a variety of nitric oxide metabolites in blood and tissues, contributing to the ability of brief periods of nitrics oxide inhalation to provide cardioprotection against ischemia–reperfusion injury.

TL;DR: Brief elevations in plasma nitrite trigger a concerted cardioprotective response characterized by persistent changes in cardiac metabolism, redox stress, and alterations in myocardial signaling, and have implications for nitrite dosing in therapeutic regimens.

TL;DR: Findings suggest that a yet unidentified source of NO, unrelated to NOSs or dietary NOx, may be sustaining basal NO signaling in tissues and may offer new therapeutic avenues for correcting NO deficiencies.