Effect of epinephrine or cAMP on cAMP-bound protein kinase holoenzymes in rat heart

1991 ◽  
Vol 260 (3) ◽  
pp. H722-H729
Author(s):  
H. Jiang ◽  
J. D. Corbin

Nonperfused or epinephrine-perfused rat hearts were used to examine the relative amounts of adenosine 3',5'-cyclic monophosphate (cAMP)-free and cAMP-bound holoenzymes of type II cAMP-dependent protein kinase (cAK). Crude tissue extracts of nonperfused hearts were chromatographed in the absence or presence of [3H]cAMP using DEAE-high-performance liquid chromatography. A partially resolved cAMP-free peak of cAK eluted at 0.17 M NaCl, and an asymmetric peak containing bound [3H]cAMP eluted at a slightly higher NaCl concentration. The first peak contained a tetrameric holoenzyme [2 regulatory (R) subunits and 2 catalytic (C) subunits]. From analysis of R-to-C ratios, the [3H]cAMP-bound peak contained a mixture of tetrameric and trimeric (R2C) forms. Both cAMP-free and cAMP-bound holoenzyme forms were virtually inactive without added cAMP under the conditions used. [3H]cAMP dissociation rate studies revealed that the bound cAMP in the peak fraction was equally distributed in the two different binding sites of the enzyme. Compared with the cAMP-free form, the cAMP-bound enzyme in the peak fraction exhibited enhanced binding in nonequilibrium [3H]cAMP binding assays. The cAMP-bound holoenzymes were estimated to represent at least 64% of the total type II cAK in control extracts, and the cAMP-free form was largely converted to the cAMP-bound forms by perfusing hearts with epinephrine.

1999 ◽  
Vol 276 (5) ◽  
pp. H1625-H1633 ◽  
Author(s):  
Meike Kuschel ◽  
Peter Karczewski ◽  
Petra Hempel ◽  
Wolfgang-Peter Schlegel ◽  
Ernst-Georg Krause ◽  
...  

Phospholamban is a critical regulator of sarcoplasmic reticulum Ca2+-ATPase and myocardial contractility. To determine the extent of cross signaling between Ca2+ and cAMP pathways, we have investigated the β-adrenergic-induced phosphorylation of Ser16 and Thr17 of phospholamban in perfused rat hearts using antibodies recognizing phospholamban phosphorylated at either position. Isoproterenol caused the dose-dependent phosphorylation of Ser16 and Thr17 with strikingly different half-maximal values (EC50 = 4.5 ± 1.6 and 28.2 ± 1.4 nmol/l, respectively). The phosphorylation of Ser16 induced by isoproterenol, forskolin, or 3-isobutyl-1-methylxanthine correlated to increased cardiac relaxation ( r = 0.96), whereas phosphorylation of Thr17 did not. Elevation of extracellular Ca2+did not induce phosphorylation at Thr17; only in the presence of a submaximal dose of isoproterenol, phosphorylation at Thr17 increased eightfold without additional effects on relaxation rate. Thr17 phosphorylation was partially affected by ryanodine and was completely abolished in the presence of 1 μmol/l verapamil or nifedipine. The data indicate that 1) phosphorylation of phospholamban at Ser16 by cAMP-dependent protein kinase is the main regulator of β-adrenergic-induced cardiac relaxation definitely preceding Thr17 phosphorylation and 2) the β-adrenergic-mediated phosphorylation of Thr17 by Ca2+-calmodulin-dependent protein kinase required influx of Ca2+through the L-type Ca2+ channel.


IUBMB Life ◽  
1996 ◽  
Vol 40 (6) ◽  
pp. 1159-1166
Author(s):  
I. D. Grozdova ◽  
N. A. Alexandrova ◽  
E. V. Sveshnikova ◽  
N. S. Melik-Nubarov ◽  
P. G. Sveshnikov ◽  
...  

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