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Specific activation of adenylyl cyclase V by a purinergic agonist
Author(s) -
Pucéat Michel,
Bony Claire,
Jaconi Marisa,
Vassort Guy
Publication year - 1998
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(98)00747-9
Subject(s) - adenylyl cyclase , agonist , purinergic receptor , chemistry , adcy9 , pharmacology , endocrinology , biochemistry , receptor , biology
The present study was designed to investigate whether and how the purinergic stimulation of rat ventricular myocytes modulates the cAMP‐dependent pathway. Stimulation of cardiomyocytes with ATPγS in the presence of the phosphodiesterase inhibitor IBMX increases by 3‐fold intracellular cAMP content. In contrast to β‐adrenergic stimulation, the purinergic stimulation of adenylyl cyclase was not inhibited by activation or enhanced by inhibition of a G i protein. Forskolin did not potentiate the effect of extracellular ATPγS on intracellular cAMP content but the effect of isoproterenol did. Like isoproterenol, the purinergic agonist decreased subsequent ADP‐ribosylation of a 45 kDa G αs by cholera toxin. ATPγS also increased cAMP content in neonatal rat cardiomyocytes, a cell type that expresses a long form of G s protein (α s , 52 kDa) in contrast to adult rat cardiomyocytes that express mostly a short form of G s protein (α s , 45 kDa). Both purinergic and β‐adrenergic agonists increased cAMP in HEK 293 cells expressing type V adenylyl cyclase while cAMP was only increased by β‐adrenergic stimulation of HEK expressing type IV or VI adenylyl cyclases. Thus, we propose that the purinergic and β‐adrenergic stimulations differentially activate adenylyl cyclase isoforms in rat cardiomyocytes and that adenylyl cyclase V is the specific target of the purinergic stimulation.