Chronic hypoxia inhibits tetrahydrobiopterin-induced NO production in rat lungs
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11130%2F13%3A10209793" target="_blank" >RIV/00216208:11130/13:10209793 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1016/j.resp.2012.11.012" target="_blank" >http://dx.doi.org/10.1016/j.resp.2012.11.012</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1016/j.resp.2012.11.012" target="_blank" >10.1016/j.resp.2012.11.012</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Chronic hypoxia inhibits tetrahydrobiopterin-induced NO production in rat lungs
Popis výsledku v původním jazyce
Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthases (NOS). Oxidative stress oxidises BH4 to dihydrobioptein (BH2), resulting in the uncoupling of the two enzymatic domains of NOS and the production of superoxide rather than NO (NOS uncoupling). Oxidative stress is known to be increased in the early stage of chronic hypoxia. This study investigated the participation of NOS uncoupling in the early phase of hypoxia-induced pulmonary hypertension in rats. Rats were exposed to 10% O-2 for 4 days. We investigated the effect of BH4 in vitro on isolated rat lungs and isolated rat peripheral pulmonary blood vessels and in vivo on exhaled NO concentration in exhaled air. BH4 attenuated hypoxic pulmonary vasoconstriction in isolated lungs and its effect was reversed by L-NAME (NOS inhibitor). The main finding of the study is that the effect of BH4 was smaller in rats exposed to 4 days of hypoxia than in normoxic controls. The finding was similar in isolated pulmonary blo
Název v anglickém jazyce
Chronic hypoxia inhibits tetrahydrobiopterin-induced NO production in rat lungs
Popis výsledku anglicky
Tetrahydrobiopterin (BH4) is an essential cofactor for nitric oxide synthases (NOS). Oxidative stress oxidises BH4 to dihydrobioptein (BH2), resulting in the uncoupling of the two enzymatic domains of NOS and the production of superoxide rather than NO (NOS uncoupling). Oxidative stress is known to be increased in the early stage of chronic hypoxia. This study investigated the participation of NOS uncoupling in the early phase of hypoxia-induced pulmonary hypertension in rats. Rats were exposed to 10% O-2 for 4 days. We investigated the effect of BH4 in vitro on isolated rat lungs and isolated rat peripheral pulmonary blood vessels and in vivo on exhaled NO concentration in exhaled air. BH4 attenuated hypoxic pulmonary vasoconstriction in isolated lungs and its effect was reversed by L-NAME (NOS inhibitor). The main finding of the study is that the effect of BH4 was smaller in rats exposed to 4 days of hypoxia than in normoxic controls. The finding was similar in isolated pulmonary blo
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
ED - Fyziologie
OECD FORD obor
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Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2013
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Respiratory Physiology and Neurobiology
ISSN
1569-9048
e-ISSN
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Svazek periodika
185
Číslo periodika v rámci svazku
3
Stát vydavatele periodika
NL - Nizozemsko
Počet stran výsledku
6
Strana od-do
547-552
Kód UT WoS článku
000315322900009
EID výsledku v databázi Scopus
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