Differential Regulation of Beta-Adrenergic Receptor-Coupled Adenylate Cyclase by Thyroid Hormones in Rat Liver and Heart: Possible Role of Corticosteroids

1987 ◽  
Vol 27 (2) ◽  
pp. 109-118 ◽  
Author(s):  
Pavur R. Sundaresan ◽  
Shailesh P. Banerjee
Science ◽  
1982 ◽  
Vol 218 (4575) ◽  
pp. 900-901 ◽  
Author(s):  
A Janowsky ◽  
F Okada ◽  
D. Manier ◽  
C. Applegate ◽  
F Sulser ◽  
...  

1985 ◽  
Vol 248 (6) ◽  
pp. E712-E718 ◽  
Author(s):  
M. S. Katz ◽  
S. R. Boland ◽  
S. J. Schmidt

beta-Adrenergic agonist-sensitive adenylate cyclase activity and binding of the beta-adrenergic antagonist(-)-[125I]iodopindolol were studied in rat liver during development of male Fischer 344 rats ages 6-60 days. In liver homogenates maximum adenylate cyclase response to beta-adrenergic agonist (10(-5) M isoproterenol or epinephrine) decreased by 73% (P less than 0.01) between 6 and 60 days, with most of the decrease (56%; P less than 0.01) occurring by 20 days. beta-adrenergic receptor density (Bmax) showed a corresponding decrease of 66% (P less than 0.01) by 20 days without subsequent change. Binding characteristics of stereospecificity, pharmacological specificity, saturability with time, and reversibility were unchanged with age. GTP-, fluoride-, forskolin-, and Mn2+-stimulated adenylate cyclase activities also decreased during development, suggesting a decrease of activity of the catalytic component and/or guanine nucleotide regulatory component of adenylate cyclase. These results indicate that the developmental decrease of beta-adrenergic agonist-sensitive adenylate cyclase activity may result from decreased numbers of beta-adrenergic receptors. Developmental alterations of nonreceptor components of the enzyme may also contribute to changes of catecholamine-sensitive adenylate cyclase.


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