Home General Physiology and Biophysics 2016 General Physiology and Biophysics Vol.35, No.2, p.165–173, 2016

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.35, No.2, p.165–173, 2016

Title: β-Adrenergic signaling in rat heart is similarly affected by continuous and intermittent normobaric hypoxia
Author: Klara Hahnova, Dita Kasparova, Jitka Zurmanova, Jan Neckar, Frantisek Kolar, Jiri Novotny
Abstract: 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.
Keywords: Rat myocardium — Chronic hypoxia — β-adrenergic receptors — Adenylyl cyclase
Published online: 10-Mar-2016
Year: 2016, Volume: 35, Issue: 2 Page From: 165, Page To: 173
doi:10.4149/gpb_2015053


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