Open Accessβ-Adrenergic signaling in rat heart is similarly affected by continuous and intermittent normobaric hypoxia
Author(s) -
Klára Hahnová,
Dita Kašparová,
Jitka Žurmanová,
Jan Neckář,
František Kolář,
Jiřı́ Novotný
Publication year - 2016
Publication title -
general physiology and biophysics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.376
H-Index - 39
eISSN - 1338-4325
pISSN - 0231-5882
DOI - 10.4149/gpb_2015053
Subject(s) - hypoxia (environmental) , adenylyl cyclase , adrenergic , medicine , endocrinology , adrenergic receptor , cardioprotection , receptor , pharmacology , biology , ischemia , chemistry , oxygen , organic chemistry
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.