作者: Birgitt Stein , Jasper Kiehn , Joachim Neumann
DOI: 10.1007/978-1-4615-5603-9_7
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摘要: A defective adenosine receptor-mediated autoregulation of the heart has been hypothesized to cause cardiomyopathy. Regulation gene expression four receptor subtypes A1, A2A, A2B, A3 and A1-mediated antiadrenergic signal transduction pathway studied in nonfailing failing human hearts. Gene myocardial A1-adenosine receptors inhibitory effects on cAMP levels or negative inotropic were not altered compared hearts, indicating that an impairment may be involved pathogenesis failure. Furthermore, A3-adenosine was unchanged while A2B mRNA detectable. However, A2A-adenosine increased by about 60% patients with dilated Thus, A2A-upregulation indicate a pathophysiological role for adds therefore increasingly complex picture molecular alterations