β-Adrenergic signaling in rat heart is similarly affected by continuous and intermittent normobaric hypoxia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F16%3A10332848" target="_blank" >RIV/00216208:11310/16:10332848 - isvavai.cz</a>

Výsledek na webu

<a href="http://hdl.handle.net/11104/0258786" target="_blank" >http://hdl.handle.net/11104/0258786</a>

DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

β-Adrenergic signaling in rat heart is similarly affected by continuous and intermittent normobaric hypoxia

Popis výsledku v původním jazyce

Chronic hypoxia may produce a cardioprotective phenotype characterized by increased resistance to ischemia-reperfusion injury. Nevertheless, the molecular basis of cardioprotective effects of hypoxia is still not quite clear. The present study investigated the consequences of a 3-week adaptation to cardioprotective (CNH, continuous normobaric hypoxia) and nonprotective (INH, intermittent normobaric hypoxia; 23 h/day hypoxia followed by 1 h/day reoxygenation) regimen of hypoxia on β-adrenergic signaling in the rat myocardium. Both regimens of hypoxia lowered body weight and led to marked right ventricular (RV) hypertrophy, which was accompanied by 25% loss of β1-adrenergic receptors (β1-ARs) in the RV. No significant changes were found in β-ARs in left ventricular (LV) preparations from animals adapted to hypoxia. Although adenylyl cyclase (AC) activity stimulated through the G proteins was decreased in the RV and increased in the LV after exposure to hypoxia, there were no significant changes in the expression of the dominant myocardial AC 5/6 isoforms and the stimulatory G proteins. These data suggest that chronic normobaric hypoxia may strongly affect myocardial β-adrenergic signaling but adaptation to cardioprotective and nonprotective regimens of hypoxia does not cause notably diverse changes.

Název v anglickém jazyce

β-Adrenergic signaling in rat heart is similarly affected by continuous and intermittent normobaric hypoxia

Popis výsledku anglicky

Chronic hypoxia may produce a cardioprotective phenotype characterized by increased resistance to ischemia-reperfusion injury. Nevertheless, the molecular basis of cardioprotective effects of hypoxia is still not quite clear. The present study investigated the consequences of a 3-week adaptation to cardioprotective (CNH, continuous normobaric hypoxia) and nonprotective (INH, intermittent normobaric hypoxia; 23 h/day hypoxia followed by 1 h/day reoxygenation) regimen of hypoxia on β-adrenergic signaling in the rat myocardium. Both regimens of hypoxia lowered body weight and led to marked right ventricular (RV) hypertrophy, which was accompanied by 25% loss of β1-adrenergic receptors (β1-ARs) in the RV. No significant changes were found in β-ARs in left ventricular (LV) preparations from animals adapted to hypoxia. Although adenylyl cyclase (AC) activity stimulated through the G proteins was decreased in the RV and increased in the LV after exposure to hypoxia, there were no significant changes in the expression of the dominant myocardial AC 5/6 isoforms and the stimulatory G proteins. These data suggest that chronic normobaric hypoxia may strongly affect myocardial β-adrenergic signaling but adaptation to cardioprotective and nonprotective regimens of hypoxia does not cause notably diverse changes.

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FA - Kardiovaskulární nemoci včetně kardiochirurgie

OECD FORD obor

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Projekt

<a href="/cs/project/GAP303%2F12%2F1162" target="_blank" >GAP303/12/1162: Interakce mezi dlouhodobými formami kardioprotekce vyvolané adaptací na chronickou hypoxii a pravidelnou fyzickou zátěží.</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

General Physiology and Biophysics

ISSN

0231-5882

e-ISSN

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Svazek periodika

2016

Číslo periodika v rámci svazku

35

Stát vydavatele periodika

SK - Slovenská republika

Počet stran výsledku

9

Strana od-do

165-173

Kód UT WoS článku

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EID výsledku v databázi Scopus

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