Expression of β-Arrestins and β-Adrenergic Receptor Kinases in the Failing Human Heart

The β-adrenergic receptor system of the failing human heart is markedly desensitized. We have recently postulated that this desensitization may in part be caused by an increase in β-adrenergic receptor kinase (βARK) expression. βARK is thought to effect desensitization by acting in concert with an inhibitor protein, called β-arrestin. Two isoforms have been identified both for βARK and for β-arrestin. In the present study, we have investigated the expression of the individual isoforms of β-arrestin and of βARK in left ventricles from failing and control human hearts. mRNAs for all four proteins, β-arrestin-1, β-arrestin-2, βARK-1, and βARK-2, were identified in human heart. Quantitation by reverse-transcription polymerase chain reactions showed that in heart failure there were no changes of the mRNA levels for β-arrestin-1 and β-arrestin-2, a slight (