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Am J Physiol Heart Circ Physiol (February 12, 2004). doi:10.1152/ajpheart.00798.2003
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Submitted on August 19, 2003
Accepted on February 11, 2004

Alterations of Adenylyl Cyclase and G-proteins in Aortocaval Shunt Induced Heart Failure

Xi Wang1, Emmanuelle Sentex1, Donald Chapman1, and Naranjan S. Dhalla1*

1 Institute of Cardiovascular Sciences and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada

* To whom correspondence should be addressed. E-mail: nsdhalla{at}sbrc.ca.

Unlike most of other experimental models of congestive heart failure, the volume overload induced by aortocaval shunt (AVS) in rats was found to exhibit enhanced {beta}- adrenoceptor ({beta}-AR) signaling. To study whether the adenylyl cyclase (AC)-G-protein system is involved in such a change, we examined cardiac AC activity and protein content as well as Gs{alpha}- and Gi{alpha}-activities, protein contents and mRNA levels in both left and right ventricles (LV and RV) at the failing stage (16 weeks post-surgery). The basal and forskolin stimulated AC activities were significantly increased in both LV and RV from the failing hearts; this change was associated with an upregulation of type V/VI AC protein. In contrast to Gpp(NH)p and NaF, the stimulatory effect of isoproterenol on AC was increased in the failing heart. Although Gs{alpha}- and Gi{alpha}-protein contents in the failing hearts were not altered, mRNA level for Gs{alpha} was decreased by 20% and that for Gi{alpha} was increased by 20%. In addition, the activity of Gs {alpha}, but not Gi{alpha}, as assessed by toxin catalyzed ADP-ribosylation, was significantly decreased in the failing heart. Losartan and imidapril treatments improved cardiac function and attenuated alterations in mRNA levels for Gs{alpha}- and Gi{alpha}-proteins, as well as Gs{alpha} activity without affecting changes in AC protein content or activities in heart failure due to volume overload. These data suggest that increased AC activity may contribute to the enhanced {beta}-AR signaling in the AVS model of heart failure whereas alterations in gene expression for G-proteins may be of adaptive nature at this stage of heart failure.




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