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.

Department of Physiology Faculty of Science Charles University Prague Prague Czech Republic

References provided by Crossref.org

Cardioprotective Effect of Chronic Hypoxia Involves Inhibition of Mitochondrial Permeability Transition Pore Opening

Continuous short-term acclimation to moderate cold elicits cardioprotection in rats, and alters β-adrenergic signaling and immune status

β-Adrenergic signaling, monoamine oxidase A and antioxidant defence in the myocardium of SHR and SHR-mtBN conplastic rat strains: the effect of chronic hypoxia

Chronic intermittent hypoxia affects the cytosolic phospholipase A2α/cyclooxygenase 2 pathway via β2-adrenoceptor-mediated ERK/p38 stimulation