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Am J Physiol Regul Integr Comp Physiol 280: R897-R903, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 3, R897-R903, March 2001

Upregulation of G protein-linked receptor kinases with advancing age in rat aorta

William E. Schutzer1, John F. Reed1, Michael Bliziotes1,2, and Scott L. Mader1,2

1 Portland Veterans Affairs Medical Center, Research Service, Portland 97201 and 2 Oregon Health Sciences University, School of Medicine, Portland, Oregon 97201

The age-related decline in beta -adrenergic receptor (beta -AR)-mediated vasorelaxation is associated with desensitization of beta -ARs without significant downregulation. The primary mode of this homologous beta -AR desensitization, in general, is via G protein receptor kinases (GRK). Therefore, we hypothesize that age-related changes in GRKs are causative to this etiology in rat aorta. Herein, we investigate the activity and cellular distribution (cytoplasmic vs. membrane) of several GRK isoforms and beta -arrestin proteins. GRK activity was assessed in extracts from aortic tissue of 6-wk, 6-mo, 12-mo, and 24-mo-old male Fischer-344 rats using a rhodopsin phosphorylation assay. We also performed immunoblots on lysates from aorta with specific antibodies to GRK-2, -3, -5, and beta -arrestin-1. Results show an age-related increase in GRK activity. Furthermore, expression of GRK-2 (cytoplasmic and membrane), GRK-3 (cytoplasmic and membrane), and beta -arrestin (soluble) increased with advancing age, whereas GRK-5 (membrane) expression remained unchanged. These results suggest that age is associated with increased activity and expression of specific GRKs. This increase likely results in enhanced phosphorylation and desensitization of beta -ARs. These biochemical changes are consistent with observed aging physiology.

beta -adrenergic receptor kinase; beta -adrenergic receptor; vasorelaxation


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