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

• Published in: General physiology and biophysics 2016-04, Vol.35 (2), p.165-173
• Main Authors: Hahnova, Klara, Kasparova, Dita, Zurmanova, Jitka, Neckar, Jan, Kolar, Frantisek, Novotny, Jiri
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological; Animals; Hypoxia - physiopathology; Male; Myocardium - metabolism; Oxygen - metabolism; Rats; Rats, Wistar; Receptors, Adrenergic, beta - metabolism; Signal Transduction
• ISSN: 0231-5882
• DOI: 10.4149/gpb_2015053

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.