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J Appl Physiol 94: 2423-2432, 2003; doi:10.1152/japplphysiol.00958.2002
8750-7587/03 $5.00
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Vol. 94, Issue 6, 2423-2432, June 2003

Altered myocardial Gs protein and adenylyl cyclase signaling in rats exposed to chronic hypoxia and normoxic recovery

Markéta Hrbasová1, Jiri Novotny1,2, Lucie Hejnová1,2, Frantisek Kolár3,4, Jan Neckár3,4, and Petr Svoboda1,2

1 Faculty of Natural Sciences, Department of Physiology and Developmental Biology, Charles University, Vinicna 7, Prague 2; 2 Biochemistry of Membrane Receptors Group and 3 Department of Developmental Cardiology, Institute of Physiology, Academy of Sciences of the Czech Republic, and 4 Centre for Experimental Cardiovascular Research, Videnska 1083, Prague 4, Czech Republic

The present work has analyzed the consequences of chronic intermittent high-altitude hypoxia for functioning of the G protein-mediated adenylyl cyclase (AC) signaling system in the right (RV) and left ventricular (LV) myocardium in rats. Adaptation to hypoxia did not appreciably affect the number of beta -adrenoceptors and the content of predominantly membrane-bound alpha -subunit (Gsalpha ) of the stimulatory G protein, but it raised the amount of cytosolic Gsalpha in RV. The levels of myocardial inhibitory Galpha protein were not altered. Activity of AC stimulated by GTP, fluoride, forskolin, or isoprotertenol was reduced by ~50% in RV from chronically hypoxic rats, and a weaker depression was also found in LV. In addition, hypoxia significantly diminished a functional activity of membrane-bound Gsalpha in both RV and LV. The RV baseline contractile function was markedly increased in chronically hypoxic animals, and its sensitivity to beta -adrenergic stimulation was decreased. Animals recovering from hypoxia for 5 wk still exhibited markedly elevated levels of cytosolic Gsalpha and significantly lower activity of AC in RV than did age-matched controls, but contractile responsiveness to beta -agonists was normal.

rat myocardium; beta-adrenoceptors; G proteins


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