Exhaled nitric oxide decreases upon acute exposure to high-altitude hypoxia

2006 ◽  
Vol 18 (2) ◽  
pp. 196-202 ◽  
Author(s):  
Daniel E. Brown ◽  
Cynthia M. Beall ◽  
Kingman P. Strohl ◽  
Phoebe S. Mills
2018 ◽  
Vol 5 (4) ◽  
pp. 516-529 ◽  
Author(s):  
Yaoxi He ◽  
Xuebin Qi ◽  
Ouzhuluobu ◽  
Shiming Liu ◽  
Jun Li ◽  
...  

ABSTRACT Nitric oxide (NO) is an important molecule for vasomotor tone, and elevated NO signaling was previously hypothesized as a unique and adaptive physiological change in highland Tibetans. However, there has been lack of NO data from Tibetans living at low altitude and lowlander immigrants living at high altitude, which is crucial to test this hypothesis. Here, through cross-altitude (1990–5018 m) and cross-population (Tibetans and Han Chinese) analyses of serum NO metabolites (NOx) of 2086 individuals, we demonstrate that although Tibetans have a higher serum NOx level compared to lowlanders, Han Chinese immigrants living at high altitude show an even higher level than Tibetans. Consequently, our data contradict the previous proposal of increased NO signaling as the unique adaptive strategy in Tibetans. Instead, Tibetans have a relatively lower circulating NOx level at high altitude. This observation is further supported by data from the hypoxic experiments using human umbilical vein endothelial cells and gene knockout mice. No difference is detected between Tibetans and Han Chinese for endothelial nitric oxide synthase (eNOS), the key enzyme for circulating NO synthesis, suggesting that eNOS itself is unlikely to be the cause. We show that other NO synthesis-related genes (e.g. GCH1) carry Tibetan-enriched mutations significantly associated with the level of circulating NOx in Tibetans. Furthermore, gene network analysis revealed that the downregulation and upregulation of NOx is possibly achieved through distinct pathways. Collectively, our findings provide novel insights into the physiological and genetic mechanisms of the evolutionary adaptation of Tibetans to high-altitude hypoxia.


2010 ◽  
Vol 49 ◽  
pp. S12
Author(s):  
Serpil Erzurum ◽  
Martin Feelisch ◽  
Cynthia Beall

2003 ◽  
Vol 94 (2) ◽  
pp. 724-732 ◽  
Author(s):  
Emmanuel M. Mbaku ◽  
Lubo Zhang ◽  
William J. Pearce ◽  
Sue P. Duckles ◽  
John Buchholz

In addition to adrenergic innervation, cerebral arteries also contain neuronal nitric oxide synthase (nNOS)-expressing nerves that augment adrenergic nerve function. We examined the impact of development and chronic high-altitude hypoxia (3,820 m) on nNOS nerve function in near-term fetal and adult sheep middle cerebral arteries (MCA). Electrical stimulation-evoked release of norepinephrine (NE) was measured with HPLC and electrochemical detection, whereas nitric oxide (NO) release was measured by chemiluminescence. An inhibitor of NO synthase, N ω-nitro-l-arginine methyl ester (l-NAME), significantly inhibited stimulation-evoked NE release in MCA from normoxic fetal and adult sheep with no effect in MCA from hypoxic animals. Addition of the NO donor S-nitroso- N-acetyl-dl-penicillamine fully reversed the effect of l-NAME in MCA from normoxic animals with no effect in MCA from hypoxic animals. Electrical stimulation caused a significant increase in NO release in MCA from normoxic animals, an effect that was blocked by the neurotoxin tetrodotoxin, whereas there was no increase in NO release in MCA from hypoxic animals. Relative abundance of nNOS as measured by Western blot analysis was similar in normoxic fetal and adult MCA. However, after hypoxic acclimitization, nNOS levels dramatically declined in both fetal and adult MCA. These data suggest that the function of nNOS nerves declines during chronic high-altitude hypoxia, a functional change that may be related to a decline in nNOS protein levels.


1993 ◽  
Vol 14 (02) ◽  
pp. 78-85 ◽  
Author(s):  
J. Férézou ◽  
J. Richalet ◽  
C. Sérougne ◽  
T. Coste ◽  
E. Wirquin ◽  
...  

2022 ◽  
Author(s):  
Feng Wang ◽  
Han Zhang ◽  
Tong Xu ◽  
Youchun Hu ◽  
Yugang Jiang

Abstract Gut microbiota bears adaptive potential to different environments, but little is known regarding its responses to acute high-altitude exposure. This study aimed to evaluate the microbial changes after acute exposure to simulated high-altitude hypoxia. C57BL/6J mice were divided into hypoxia and normoxia groups. The hypoxia group was exposed to a simulated altitude of 5500 m for 24 hours above sea level. The normoxia group was maintained in low-altitude of 10 m above sea level. Colonic microbiota was analyzed using 16S rRNA V4 gene sequencing. Compared with the normoxia group, shannon, simpson and Akkermansia were significantly increased, while Firmicutes to Bacteroidetes ratio and Bifidobacterium were significantly decreased in the hypoxia group. The hypoxia group exhibited lower mobile element containing and higher potentially pathogenic and stress tolerant phenotypes than those in the normoxia group. Functional analysis indicated that environmental information processing was significantly lower, metabolism, cellular processes and organismal systems were significantly higher in the hypoxia group than those in the normoxia group. In conclusion, acute exposure to simulated high-altitude hypoxia alters gut microbiota diversity and composition, which may provide a potential target to alleviate acute high-altitude diseases.


2019 ◽  
Vol 102 (5) ◽  
pp. 4606-4618 ◽  
Author(s):  
Zhiwei Kong ◽  
Chuanshe Zhou ◽  
Bin Li ◽  
Jinzhen Jiao ◽  
Liang Chen ◽  
...  

Author(s):  
Manjula Miglani ◽  
Qadar Pasha ◽  
Archana Gupta ◽  
Anjali Priyadarshini ◽  
Ramendra Pati Pandey ◽  
...  

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