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Role of H 2 O 2 in changing β-adrenoceptor and adenylyl cyclase in ischemia-reperfused hearts



In view of the accumulation of H 2 O 2 in the myocardium due to ischemia-reperfusion and changes in β-adrenoceptor mechanisms in the ischemic-reperfused heart, we investigated the effects of H 2 O 2 on the β-adrenoceptor, G-protein and adenylyl cyclase complex. Rat hearts were perfused with 1 mM H 2 O 2 for 10 min before isolating membranes for measuring the biochemical activities. The stimulation of adenylyl cyclase by different concentrations of isoproterenol was depressed upon perfusing hearts with H 2 O 2 . Both the affinity and density of β 1 -adrenoceptors as well as the density of the β 2 -adrenoceptors were decreased whereas the affinity of β 2 -adrenoceptors was increased by H 2 O 2 perfusion. Competition curves did not reveal any effect of H 2 O 2 on the proportion of coupled receptors in the high affinity state. The basal as well as forskolin-, NaF- and Gpp(NH)p-stimulated adenylyl cyclase activities were depressed by perfusing the heart with H 2 O 2 . Catalase alone or in combination with mannitol was able to significantly decrease the magnitude of alterations due to H 2 O 2 . The positive inotropic effect of 1 μM isoproterenol was markedly attenuated upon perfusing hearts with 200-500 μM H 2 O 2 for 10 min. These results suggest that H 2 O 2 may depress the β 1 -adrenoceptor, G s -proteins and catalytic subunit of the adenylyl cyclase enzyme and thus may play an important role in attenuating the β-adrenoceptor linked signal transduction due to ischemia-reperfusion injury.



Molecular and Cellular BiochemistrySpringer Journals

Published: Sep 1, 1998

DOI: 10.1023/A:1006823531286

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