Abstract:
BACKGROUND:The effect of isoproterenol on increasing the peak amplitude of the L-type calcium current is reduced in myocytes dispersed from the epicardial border zone (EBZ) of the 5-day infarcted canine heart when compared with control cells from noninfarcted hearts. This suggests that specific alterations in the beta-adrenergic receptor complex develop in this setting. The present study is an examination of individual components of the beta-adrenergic receptor complex with the aim of elucidating the biochemical defect(s) that might be responsible for the diminished beta-adrenergic receptor responsiveness in the myocytes that survive in the infarcted heart. METHODS AND RESULTS:We compared components of the beta-adrenergic receptor signaling pathway in membranes prepared from the EBZ of the 5-day infarcted heart and a remote, noninfarcted region (RZ) of the same ventricle as well as the corresponding regions of noninfarcted ventricles. Defects in multiple components of the beta-adrenergic receptor complex were confined to the EBZ of the 5-day infarcted heart. These include a decrease in beta-adrenergic receptor density; diminished basal, guanine nucleotide-, isoproterenol-, forskolin-, and manganese-dependent adenylyl cyclase activities; an increase in the EC50 for isoproterenol-dependent activation of adenylyl cyclase; a diminished level of the alpha-subunit of the Gs protein. and an elevated level of the alpha-subunit of the Gi protein. CONCLUSIONS:Defects in multiple components of the membrane beta-adrenergic receptor complex were identified in the EBZ of the 5-day infarcted canine heart. This constellation of abnormalities would be predicted to impair functional beta-adrenergic responsiveness and contribute to the defect in isoproterenol-dependent stimulation of the L-type calcium current in myocytes isolated from this tissue.
journal_name
Circulationjournal_title
Circulationauthors
Steinberg SF,Zhang H,Pak E,Pagnotta G,Boyden PAdoi
10.1161/01.cir.91.11.2824subject
Has Abstractpub_date
1995-06-01 00:00:00pages
2824-33issue
11eissn
0009-7322issn
1524-4539journal_volume
91pub_type
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