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- W953480326 abstract "A defective adenosine receptor-mediated autoregulation of the heart has been hypothesized to cause cardiomyopathy. Regulation of gene expression of the four adenosine receptor subtypes A1, A2A, A2B, A3 and the A1-mediated antiadrenergic signal transduction pathway has been studied in nonfailing and failing human hearts. Gene expression of myocardial A1-adenosine receptors and A1-mediated inhibitory effects on cAMP levels or negative inotropic effects were not altered in failing compared to nonfailing human hearts, indicating that an impairment in the A1-mediated pathway may not be involved in the pathogenesis of heart failure. Furthermore, A3-adenosine receptor gene expression was unchanged in failing compared to nonfailing hearts, while A2B mRNA was not detectable. However, A2A-adenosine receptor gene expression was increased by about 60% in patients with dilated cardiomyopathy. Thus, the A2A-upregulation may indicate a pathophysiological role for adenosine and adds therefore to the increasingly complex picture of molecular alterations in heart failure." @default.
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- W953480326 date "1998-01-01" @default.
- W953480326 modified "2023-09-26" @default.
- W953480326 title "Regulation of Adenosine Receptor Subtypes and Cardiac Dysfunction in Human Heart Failure" @default.
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- W953480326 doi "https://doi.org/10.1007/978-1-4615-5603-9_7" @default.
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