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Am J Physiol Heart Circ Physiol (February 25, 2005). doi:10.1152/ajpheart.00066.2005
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Submitted on January 24, 2005
Accepted on February 23, 2005

Upregulation of {beta}-Adrenergic Receptors in Heart Failure Due to Volume Overload

Xi Wang1, Emmanuelle Sentex1, Harjot K Saini1, Donald Chapman1, and Naranjan S Dhalla1*

1 Physiology, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center, University of Manitoba, Winnipeg, Manitoba, Canada

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

In order to examine the mechanisms of changes in {beta}-adrenergic signal transduction in heart failure due to volume overload, we studied the status of {beta}-adrenoceptors ({beta}ARs), G-protein-coupled receptor kinase (GRK) and {beta}-arrestin in hearts failing due to aortocaval shunt (AVS). Heart failure in rats was induced by creating AVS for 16 weeks and {beta}AR binding, GRK activity, as well as their protein content and mRNA levels were determined in both left and right ventricles. The density and protein content for {beta}1ARs, unlike those for {beta}2ARs, were increased in the failing hearts. Furthermore, protein contents for GRK isoforms and {beta}-arrestin1 were decreased in membranous and increased in cytosolic fractions from the failing hearts. On the other hand, steady state mRNA levels for {beta}1ARs and GRK2 as well as protein content for G[[beta]]{gamma} subunits did not change in the failing heart. Basal cardiac function was depressed; however, both in vivo and ex vivo positive inotropic responses of the failing hearts to isoproterenol were augmented. Treatment of AVS animals with imidapril (1 mg/kg/day) or losartan (20 mg/kg/day) retarded the progression of heart failure, partially prevented changes in {beta}1ARs, GRKs and {beta}-arrestin1 in the failing myocardium, and attenuated the increase in positive inotropic effect of isoproterenol. These results indicate that upregulation of {beta}1ARs is associated with subcellular redistribution of GRKs and {beta}-arrestin1 in the failing heart due to volume overload. Furthermore, attenuation of alterations in {beta}-adrenergic system by imidapril or losartan may be due to blockade of the renin-angiotensin system in the AVS model of heart failure.




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